Can human brain memory be removed by EMP?

The human brain is the most complicated human organ so it is hard to examine it completely but based on what we know do you think (or do you know from some source) if a human memory can be removed by emp(electromagnetic pulse) ? (If so do you think it would be pernament or temporary?) mentions the following natural sources of EMP, which I have ordered by frequency / period, from the shortest to the longest:

  1. Electrostatic discharge from objects coming into contact (normally too small to be of any concern)

  2. Lightning (milliseconds)

  3. Solar flares (hours.) Such flares cause geomagnetic storms (more on this later.)

Several artificial sources of EMP are mentioned, of which the only ones of interest are military:

  1. Non-nuclear weapons. The page links to a general article on directed-energy weapons, which mentions microwave devices for causing pain and for targeted damaging of electronic equipment.

  2. Nuclear weapons. gives more information on this, listing three phases.

The EMP produced by the Compton electrons typically lasts for about 1 microsecond, and this signal is called HEMP. In addition to the prompt EMP, scattered gammas and inelastic gammas produced by weapon neutrons produce an “intermediate time” signal from about 1 microsecond to 1 second. The energetic debris entering the ionosphere produces ionization and heating of the E-region. In turn, this causes the geomagnetic field to “heave,” producing a “late-time” magnetohydrodynamic (MHD) EMP generally called a heave signal.

The same reference also indicates:

… the region where the greatest damage can be produced is from about 3 to 8 km from ground zero. In this same region structures housing electrical equipment are also likely to be severely damaged by blast and shock.

As far as I am aware, memory loss was not a major recorded symptom among the survivors of Hiroshima and Nagasaki. The only recent data for sufferers of EMP would be from victims of lightning stikes. While the frequency spectrum is admittedly different from nuclear weapons, victims of lightning strikes are surely subjected to greater magnitudes of EMP than those who managed to survive nuclear bombings (who suffered many other traumas, such as blast waves and radiation.) Those who survive the immediate physical (burns) and neurological (cardiac arrest) effects of lightning strikes must surely be knocked unconscious and be disorientated when they regain consciousness. But again, I am not aware of medium or long term memory loss being a particular symptom.

It is worth comparing the structure of the brain (a fairly homogenous mass of tissue of high water content, relatively conductive) with the structure of electronic equipment (components of ever smaller size and greater resistance in order to save power, surrounded by a nonconductive medium such as air, and interconnected by wires, which serve to channel voltage.) It is unsurprising that the brain is less subsceptible to electrostatic damage than electronic components (electronics workers have to take precautions in order to avoid damaging sensitive components with static discharges from their bodies and clothing.)

The most widespread damage to equipment caused by EMP is from the long-period pulses, which are channeled by electric cables. These act over distances much larger than the size of the human body.

From the last reference:

… distortion of the geomagnetic field was observed worldwide in the case of the STARFISH test… the signal from this process is not large, but systems connected to long lines (e.g., power lines, telephone wires, and tracking wire antennas) are at risk


The first recorded EMP incident… nuclear test over the South Pacific… resulted in power system failures as far away as Hawaii. mentions cases of damage caused by long period EMP, including electric shocks suffered by telegraph operators during solar flare events.

So in conclusion, any amnesia caused by EMP is likely to be caused by normal biological shock mechanisms to individuals unfortunate enough to be electrocuted, and not by any direct electrical effect on the brain itself.

The brain is not an electronic device.

An EMP is basically a large amount of electrons flying by all at once. They are negatively charged, and as they pass by they distort your local EM-field (hence the name). This distortion induces current in the wires (a phenomenon known since Faraday) - since most wires aren't made with a large tolerance, the sudden current spike overheats the wire and burns components. In the brain, there are no wires to induce current on.

It is true that electromagnetism plays a role in neuron function, and action potentials can be measured or manipulated with electrodes. However, this is just a consequence of the ion concentration being used for signaling - there is not a flow of electrons across a conducting wire that is driving the process.

Memory is not stored electrically. The two major mechanisms of memory are strengthening of the synapses and the chemical state of the neurons (metabolites and proteins such as cAMP or CaMK, RNA levels, DNA methylation). These aren't very sensitive to electrons moving past - you're essentially trying to catalyze a chemical reaction by applying a strong EM field outside of the beaker.

Also, I suspect the skull and tissue surrounding it may act as a Faraday cage to shield the brain itself from the EM field.

I'm sure it is possible to create an electron flux so heavy that it manages to induce enough current in cells to kill them (or current in your bloodstream to cause cardiac arrest). However, the nuclear explosion that produces this would probably be much deadlier due to other effects, like blast shockwave or gamma rays. So to answer your question, a nuclear EMP would either kill you or not affect your memories, although if you had some exotic, very powerful, very precise pure EMP generator perhaps you could get some sort of stunning effect or give people a headache. I don't think it could erase memories without killing large parts of the brain.

This isn't a ridiculous idea; Transcranial Magnetic Stimulation is used in research and even has some use as treatment for depression (

In TMS a strong, localized magnetic field can disrupt normal functioning of regions of the brain. For instance it can be used on the visual cortex to cause temporary blindness (actually, can cause a condition called blindsight:

As for memory though, TMS does not seem to be able to cause permanent memory loss (in fact, there is research indicating that it may be able to boost memory). Plus, the magnetic pulse would have to be either extremely strong, or very close, for it to have an appreciable effect.

How Human Memory Works

There you are at a business function and you see a colleague across the room. As you walk over, you suddenly realize you can't remember the person's name. Odds are you're not suddenly developing Alzheimer's disease, although many people jump to that conclusion. You're simply experiencing a breakdown of the assembly process of memory -- a breakdown that many of us begin to experience in our 20s and that tends to get worse as we reach our 50s. This age-dependent loss of function appears in many animals, and it begins with the onset of sexual maturity.

We saw earlier in this chapter that as you learn and remember, your brain doesn't change its overall structure or grow whole new batches of nerve cells -- it's the connections between cells that change as you learn. Your synapses are reinforced, and cells make more and stronger connections with each other. But as you begin to age, these synapses begin to falter, which begins to affect how easily you can retrieve memories.

Researchers have several theories about what's behind this deterioration, but most suspect that aging causes major cell loss in a tiny region in the front of the brain that leads to a drop in the production of a neurotransmitter called acetylcholine. Acetylcholine is vital to learning and memory.

In addition, some parts of the brain that are essential to memory are highly vulnerable to aging. One area, called the hippocampus, loses 5 percent of its nerve cells with each passing decade -- for a total loss of 20 percent by the time you reach your 80s. In addition, the brain itself shrinks and becomes less efficient as you age.

Of course, other things can happen to your brain to speed up this decline. You may have inherited some unhealthy genes, you might have been exposed to poisons, or perhaps you smoked or drank too much. All these things speed up memory decline.

So you can see that as you age, some physical changes in the brain can make it more difficult to remember efficiently. The good news is that this doesn't mean that memory loss and dementia are inevitable. While some specific abilities do decline with age, overall memory remains strong for most people throughout their 70s. In fact, research shows that the average 70-year-old performs as well on certain cognitive tests as do many 20-year-olds, and many people in their 60s and 70s score significantly better in verbal intelligence than do younger people.

Studies also have shown that many of the memory problems experienced by older people can be lessened -- or even reversed. Studies of nursing-home populations show that patients were able to make significant improvements in memory when given rewards and challenges. Physical exercise and mental stimulation also can really improve mental function.

Evidence from animal studies suggests that stimulating the brain can stop cells from shrinking and can even increase brain size in some cases. Studies show that rats living in enriched environments with lots of toys and challenges have larger outer brains with larger, healthier brain cells. And animals given lots of mental exercise have more dendrites, which allow their cells to communicate with each other. Research has shown that, in our later years, a stimulating environment encourages the growth of these dendrites, while a dull environment impedes it.

The important point to remember is that as you age, you may not learn or remember as quickly as you did when you were in school -- but you will likely learn and remember nearly as well. In many cases, an older person's brain may be less effective not because of a structural or organic problem but simply as a result of lack of use.

Richard C. Mohs, Ph.D., has been vice chairman of the Department of Psychiatry at the Mount Sinai School of Medicine and associate chief of staff for research at the Bronx Veterans Affairs Medical Center. The author or co-author of more than 300 scientific papers, Dr. Mohs has conducted numerous research studies on aging, Alzheimer's disease, and cognitive function.

Carol Turkington is a freelance writer who specializes in the fields of health and psychology. A former editor and writer for the Duke University Medical Center and the American Psychological Association, she has more than 40 books to her credit, including The Memory and Memory Disorders Sourcebook The Encyclopedia of Memory and Memory Disorders and The Brain Encyclopedia.

Making Memories

On a late summer day in 1953, a young man who would soon be known as patient H.M. underwent experimental surgery. In an attempt to treat his debilitating seizures, a surgeon removed portions of his brain, including part of a structure called the hippocampus. The seizures stopped.

Unfortunately, for patient H.M., so too did time. When he woke up after surgery, he could no longer form new long-term memories, despite retaining normal cognitive abilities, language and short-term working memory. Patient H.M.’s condition ultimately revealed that the brain’s ability to create long-term memories is a distinct process that depends on the hippocampus.

Scientists had discovered where memories are made. But how they are made remained unknown.

Now, neuroscientists at Harvard Medical School have taken a decisive step in the quest to understand the biology of long-term memory and find ways to intervene when memory deficits occur with age or disease.

Reporting in Nature on Dec. 9, they describe a newly identified mechanism that neurons in the adult mouse hippocampus use to regulate signals they receive from other neurons, in a process that appears critical for memory consolidation and recall.

The study was led by Lynn Yap, HMS graduate student in neurobiology, and Michael Greenberg, chair of neurobiology in the Blavatnik Institute at HMS.

“Memory is essential to all aspects of human existence. The question of how we encode memories that last a lifetime is a fundamental one, and our study gets to the very heart of this phenomenon,” said Greenberg, the HMS Nathan Marsh Pusey Professor of Neurobiology and study corresponding author.

The researchers observed that new experiences activate sparse populations of neurons in the hippocampus that express two genes, Fos and Scg2. These genes allow neurons to fine-tune inputs from so-called inhibitory interneurons, cells that dampen neuronal excitation. In this way, small groups of disparate neurons may form persistent networks with coordinated activity in response to an experience.

“This mechanism likely allows neurons to better talk to each other so that the next time a memory needs to be recalled, the neurons fire more synchronously,” Yap said. “We think coincident activation of this Fos-mediated circuit is potentially a necessary feature for memory consolidation, for example, during sleep, and also memory recall in the brain.”

Circuit orchestration

In order to form memories, the brain must somehow wire an experience into neurons so that when these neurons are reactivated, the initial experience can be recalled. In their study, Greenberg, Yap and team set out to explore this process by looking at the gene Fos.

First described in neuronal cells by Greenberg and colleagues in 1986, Fos is expressed within minutes after a neuron is activated. Scientists have taken advantage of this property, using Fos as a marker of recent neuronal activity to identify brain cells that regulate thirst, torpor and many other behaviors.

Scientists hypothesized that Fos might play a critical role in learning and memory, but for decades, the precise function of the gene has remained a mystery.

To investigate, the researchers exposed mice to new environments and looked at pyramidal neurons, the principal cells of the hippocampus. They found that relatively sparse populations of neurons expressed Fos after exposure to a new experience. Next, they prevented these neurons from expressing Fos, using a virus-based tool delivered to a specific area of the hippocampus, which left other cells unaffected.

Mice that had Fos blocked in this manner showed significant memory deficits when assessed in a maze that required them to recall spatial details, indicating that the gene plays a critical role in memory formation.

After exposure to a novel environment, a sparse population of neurons in the mouse hippocampus express Fos (red). Image: Yap and colleagues

The researchers studied the differences between neurons that expressed Fos and those that did not. Using optogenetics to turn inputs from different nearby neurons on or off, they discovered that the activity of Fos-expressing neurons was most strongly affected by two types of interneurons.

Neurons expressing Fos were found to receive increased activity-dampening, or inhibitory, signals from one distinct type of interneuron and decreased inhibitory signals from another type. These signaling patterns disappeared in neurons with blocked Fos expression.

“What’s critical about these interneurons is that they can regulate when and how much individual Fos-activated neurons fire, and also when they fire relative to other neurons in the circuit,” Yap said. “We think that at long last we have a handle on how Fos may in fact support memory processes, specifically by orchestrating this type of circuit plasticity in the hippocampus.”

Imagine the day

The researchers further probed the function of Fos, which codes for a transcription factor protein that regulates other genes. They used single-cell sequencing and additional genomic screens to identify genes activated by Fos and found that one gene in particular, Scg2, played a critical role in regulating inhibitory signals.

In mice with experimentally silenced Scg2, Fos-activated neurons in the hippocampus displayed a defect in signaling from both types of interneurons. These mice also had defects in theta and gamma rhythms, brain properties thought to be critical features of learning and memory.

Previous studies had shown that Scg2 codes for a neuropeptide protein that can be cleaved into four distinct forms, which are then secreted. In the current study, Yap and colleagues discovered that neurons appear to use these neuropeptides to fine-tune inputs they receive from interneurons.

Together, the team’s experiments suggest that after a new experience, a small group of neurons simultaneously express Fos, activating Scg2 and its derived neuropeptides, in order to establish a coordinated network with its activity regulated by interneurons.

“When neurons are activated in the hippocampus after a new experience, they aren’t necessarily linked together in any particular way in advance,” Greenberg said. “But interneurons have very broad axonal arbors, meaning they can connect with and signal to many cells at once. This may be how a sparse group of neurons can be linked together to ultimately encode a memory.”

The study findings represent a possible molecular- and circuit-level mechanism for long-term memory. They shed new light on the fundamental biology of memory formation and have broad implications for diseases of memory dysfunction.

The researchers note, however, that while the results are an important step in our understanding of the inner workings of memory, numerous unanswered questions about the newly identified mechanisms remain.

“We’re not quite at the answer yet, but we can now see many of the next steps that need to be taken,” Greenberg said. “If we can better understand this process, we will have new handles on memory and how to intervene when things go wrong, whether in age-related memory loss or neurodegenerative disorders such as Alzheimer’s disease.”

The findings also represent the culmination of decades of research, even as they open new avenues of study that will likely take decades more to explore, Greenberg added.

“I arrived at Harvard in 1986, just as my paper describing the discovery that neuronal activity can turn on genes was published,” he said. “Since that time, I've been imagining the day when we would figure out how genes like Fos might contribute to long-term memory.”

Additional authors include Noah Pettit, Christopher Davis, M. Aurel Nagy, David Harmin, Emily Golden, Onur Dagliyan, Cindy Lin, Stephanie Rudolph, Nikhil Sharma, Eric Griffith and Christopher Harvey.

Neurotransmission is the interaction between these. From the neuron, the neurotransmitter is released (particularly from its axon) and interacts with the dendrites of another neuron.

They are produced in the ribosomes of the presynaptic neuron. They are stored in vesicles. These vesicle's location is cytoplasm of a neuron. When an action potential arrives at the pre-synaptic terminal, there is the entry of the calcium ions in pre-synaptic neurons.

Now, after calcium ions entry into the cell, synaptic vesicles merge with pre-synaptic membrane and neurotransmitter is released into the synaptic cleft. When neurotransmitter arrives at the cell membrane of a post-synaptic neuron, certain protein molecules are activated. These protein molecules are receptors for neurotransmitters. (2)

After binding with
receptors, neurotransmitters have two effects on the post-synaptic membrane.

Excitation of the
postsynaptic membrane or its inhibition. During excitation, an action potential
is generated. During inhibition, an action potential is inhibited.

Neurotransmitters are
released in small amounts and produce minimal excitatory or inhibitory effects.
This process takes place regardless of the action potential generated or not.
This process is amplified when an action potential arrives and the required
message is sent from neuron to its target through neurotransmission.


Sensory memory holds information, derived from the senses, less than one second after an item is perceived. The ability to look at an item and remember what it looked like with just a split second of observation, or memorization, is the example of sensory memory. It is out of cognitive control and is an automatic response. With very short presentations, participants often report that they seem to "see" more than they can actually report. The first precise experiments exploring this form of sensory memory were conducted by George Sperling (1963) [24] using the "partial report paradigm." Subjects were presented with a grid of 12 letters, arranged into three rows of four. After a brief presentation, subjects were then played either a high, medium or low tone, cuing them which of the rows to report. Based on these partial report experiments, Sperling was able to show that the capacity of sensory memory was approximately 12 items, but that it degraded very quickly (within a few hundred milliseconds). Because this form of memory degrades so quickly, participants would see the display but be unable to report all of the items (12 in the "whole report" procedure) before they decayed. This type of memory cannot be prolonged via rehearsal.

Three types of sensory memories exist. Iconic memory is a fast decaying store of visual information, a type of sensory memory that briefly stores an image that has been perceived for a small duration. Echoic memory is a fast decaying store of auditory information, also a sensory memory that briefly stores sounds that have been perceived for short durations. [25] Haptic memory is a type of sensory memory that represents a database for touch stimuli.

Short-term memory is also known as working memory. Short-term memory allows recall for a period of several seconds to a minute without rehearsal. Its capacity, however, is very limited. In 1956, George A. Miller (1920-2012), when working at Bell Laboratories, conducted experiments showing that the store of short-term memory was 7±2 items. (Hence, the title of his famous paper, "The Magical Number 7±2.") Modern estimates of the capacity of short-term memory are lower, typically of the order of 4–5 items [26] however, memory capacity can be increased through a process called chunking. [27] For example, in recalling a ten-digit telephone number, a person could chunk the digits into three groups: first, the area code (such as 123), then a three-digit chunk (456), and, last, a four-digit chunk (7890). This method of remembering telephone numbers is far more effective than attempting to remember a string of 10 digits this is because we are able to chunk the information into meaningful groups of numbers. This is reflected in some countries' tendencies to display telephone numbers as several chunks of two to four numbers.

Short-term memory is believed to rely mostly on an acoustic code for storing information, and to a lesser extent on a visual code. Conrad (1964) [28] found that test subjects had more difficulty recalling collections of letters that were acoustically similar, e.g., E, P, D. Confusion with recalling acoustically similar letters rather than visually similar letters implies that the letters were encoded acoustically. Conrad's (1964) study, however, deals with the encoding of written text thus, while memory of written language may rely on acoustic components, generalizations to all forms of memory cannot be made.

The storage in sensory memory and short-term memory generally has a strictly limited capacity and duration, which means that information is not retained indefinitely. By contrast, long-term memory can store much larger quantities of information for potentially unlimited duration (sometimes a whole life span). Its capacity is immeasurable. For example, given a random seven-digit number, one may remember it for only a few seconds before forgetting, suggesting it was stored in short-term memory. On the other hand, one can remember telephone numbers for many years through repetition this information is said to be stored in long-term memory.

While short-term memory encodes information acoustically, long-term memory encodes it semantically: Baddeley (1966) [29] discovered that, after 20 minutes, test subjects had the most difficulty recalling a collection of words that had similar meanings (e.g. big, large, great, huge) long-term. Another part of long-term memory is episodic memory, "which attempts to capture information such as 'what', 'when' and 'where ' ". [30] With episodic memory, individuals are able to recall specific events such as birthday parties and weddings.

Short-term memory is supported by transient patterns of neuronal communication, dependent on regions of the frontal lobe (especially dorsolateral prefrontal cortex) and the parietal lobe. Long-term memory, on the other hand, is maintained by more stable and permanent changes in neural connections widely spread throughout the brain. The hippocampus is essential (for learning new information) to the consolidation of information from short-term to long-term memory, although it does not seem to store information itself. It was thought that without the hippocampus new memories were unable to be stored into long-term memory and that there would be a very short attention span, as first gleaned from patient Henry Molaison [31] after what was thought to be the full removal of both his hippocampi. More recent examination of his brain, post-mortem, shows that the hippocampus was more intact than first thought, throwing theories drawn from the initial data into question. The hippocampus may be involved in changing neural connections for a period of three months or more after the initial learning.

Research has suggested that long-term memory storage in humans may be maintained by DNA methylation, [32] and the 'prion' gene. [33] [34]

Multi-store model Edit

The multi-store model (also known as Atkinson–Shiffrin memory model) was first described in 1968 by Atkinson and Shiffrin.

The multi-store model has been criticised for being too simplistic. For instance, long-term memory is believed to be actually made up of multiple subcomponents, such as episodic and procedural memory. It also proposes that rehearsal is the only mechanism by which information eventually reaches long-term storage, but evidence shows us capable of remembering things without rehearsal.

The model also shows all the memory stores as being a single unit whereas research into this shows differently. For example, short-term memory can be broken up into different units such as visual information and acoustic information. In a study by Zlonoga and Gerber (1986), patient 'KF' demonstrated certain deviations from the Atkinson–Shiffrin model. Patient KF was brain damaged, displaying difficulties regarding short-term memory. Recognition of sounds such as spoken numbers, letters, words and easily identifiable noises (such as doorbells and cats meowing) were all impacted. Visual short-term memory was unaffected, suggesting a dichotomy between visual and audial memory. [35]

Working memory Edit

In 1974 Baddeley and Hitch proposed a "working memory model" that replaced the general concept of short-term memory with an active maintenance of information in the short-term storage. In this model, working memory consists of three basic stores: the central executive, the phonological loop and the visuo-spatial sketchpad. In 2000 this model was expanded with the multimodal episodic buffer (Baddeley's model of working memory). [36]

The central executive essentially acts as an attention sensory store. It channels information to the three component processes: the phonological loop, the visuo-spatial sketchpad, and the episodic buffer.

The phonological loop stores auditory information by silently rehearsing sounds or words in a continuous loop: the articulatory process (for example the repetition of a telephone number over and over again). A short list of data is easier to remember.

The visuospatial sketchpad stores visual and spatial information. It is engaged when performing spatial tasks (such as judging distances) or visual ones (such as counting the windows on a house or imagining images).

The episodic buffer is dedicated to linking information across domains to form integrated units of visual, spatial, and verbal information and chronological ordering (e.g., the memory of a story or a movie scene). The episodic buffer is also assumed to have links to long-term memory and semantical meaning.

The working memory model explains many practical observations, such as why it is easier to do two different tasks (one verbal and one visual) than two similar tasks (e.g., two visual), and the aforementioned word-length effect. Working memory is also the premise for what allows us to do everyday activities involving thought. It is the section of memory where we carry out thought processes and use them to learn and reason about topics. [36]

Researchers distinguish between recognition and recall memory. Recognition memory tasks require individuals to indicate whether they have encountered a stimulus (such as a picture or a word) before. Recall memory tasks require participants to retrieve previously learned information. For example, individuals might be asked to produce a series of actions they have seen before or to say a list of words they have heard before.

By information type Edit

Topographical memory involves the ability to orient oneself in space, to recognize and follow an itinerary, or to recognize familiar places. [37] Getting lost when traveling alone is an example of the failure of topographic memory. [38]

Flashbulb memories are clear episodic memories of unique and highly emotional events. [39] People remembering where they were or what they were doing when they first heard the news of President Kennedy's assassination, [40] the Sydney Siege or of 9/11 are examples of flashbulb memories.

Anderson (1976) [41] divides long-term memory into declarative (explicit) and procedural (implicit) memories.

Declarative Edit

Declarative memory requires conscious recall, in that some conscious process must call back the information. It is sometimes called explicit memory, since it consists of information that is explicitly stored and retrieved. Declarative memory can be further sub-divided into semantic memory, concerning principles and facts taken independent of context and episodic memory, concerning information specific to a particular context, such as a time and place. Semantic memory allows the encoding of abstract knowledge about the world, such as "Paris is the capital of France". Episodic memory, on the other hand, is used for more personal memories, such as the sensations, emotions, and personal associations of a particular place or time. Episodic memories often reflect the "firsts" in life such as a first kiss, first day of school or first time winning a championship. These are key events in one's life that can be remembered clearly.

Research suggests that declarative memory is supported by several functions of the medial temporal lobe system which includes the hippocampus. [42] Autobiographical memory – memory for particular events within one's own life – is generally viewed as either equivalent to, or a subset of, episodic memory. Visual memory is part of memory preserving some characteristics of our senses pertaining to visual experience. One is able to place in memory information that resembles objects, places, animals or people in sort of a mental image. Visual memory can result in priming and it is assumed some kind of perceptual representational system underlies this phenomenon. [42]

Procedural Edit

In contrast, procedural memory (or implicit memory) is not based on the conscious recall of information, but on implicit learning. It can best be summarized as remembering how to do something. Procedural memory is primarily used in learning motor skills and can be considered a subset of implicit memory. It is revealed when one does better in a given task due only to repetition – no new explicit memories have been formed, but one is unconsciously accessing aspects of those previous experiences. Procedural memory involved in motor learning depends on the cerebellum and basal ganglia. [43]

A characteristic of procedural memory is that the things remembered are automatically translated into actions, and thus sometimes difficult to describe. Some examples of procedural memory include the ability to ride a bike or tie shoelaces. [44]

By temporal direction Edit

Another major way to distinguish different memory functions is whether the content to be remembered is in the past, retrospective memory, or in the future, prospective memory. John Meacham introduced this distinction in a paper presented at the 1975 American Psychological Association annual meeting and subsequently included by Ulric Neisser in his 1982 edited volume, Memory Observed: Remembering in Natural Contexts. [45] [46] [47] Thus, retrospective memory as a category includes semantic, episodic and autobiographical memory. In contrast, prospective memory is memory for future intentions, or remembering to remember (Winograd, 1988). Prospective memory can be further broken down into event- and time-based prospective remembering. Time-based prospective memories are triggered by a time-cue, such as going to the doctor (action) at 4pm (cue). Event-based prospective memories are intentions triggered by cues, such as remembering to post a letter (action) after seeing a mailbox (cue). Cues do not need to be related to the action (as the mailbox/letter example), and lists, sticky-notes, knotted handkerchiefs, or string around the finger all exemplify cues that people use as strategies to enhance prospective memory.

To assess infants Edit

Infants do not have the language ability to report on their memories and so verbal reports cannot be used to assess very young children's memory. Throughout the years, however, researchers have adapted and developed a number of measures for assessing both infants' recognition memory and their recall memory. Habituation and operant conditioning techniques have been used to assess infants' recognition memory and the deferred and elicited imitation techniques have been used to assess infants' recall memory.

Techniques used to assess infants' recognition memory include the following:

  • Visual paired comparison procedure (relies on habituation): infants are first presented with pairs of visual stimuli, such as two black-and-white photos of human faces, for a fixed amount of time then, after being familiarized with the two photos, they are presented with the "familiar" photo and a new photo. The time spent looking at each photo is recorded. Looking longer at the new photo indicates that they remember the "familiar" one. Studies using this procedure have found that 5- to 6-month-olds can retain information for as long as fourteen days. [48]
  • Operant conditioning technique: infants are placed in a crib and a ribbon that is connected to a mobile overhead is tied to one of their feet. Infants notice that when they kick their foot the mobile moves – the rate of kicking increases dramatically within minutes. Studies using this technique have revealed that infants' memory substantially improves over the first 18-months. Whereas 2- to 3-month-olds can retain an operant response (such as activating the mobile by kicking their foot) for a week, 6-month-olds can retain it for two weeks, and 18-month-olds can retain a similar operant response for as long as 13 weeks. [49][50][51]

Techniques used to assess infants' recall memory include the following:

  • Deferred imitation technique: an experimenter shows infants a unique sequence of actions (such as using a stick to push a button on a box) and then, after a delay, asks the infants to imitate the actions. Studies using deferred imitation have shown that 14-month-olds' memories for the sequence of actions can last for as long as four months. [52]
  • Elicited imitation technique: is very similar to the deferred imitation technique the difference is that infants are allowed to imitate the actions before the delay. Studies using the elicited imitation technique have shown that 20-month-olds can recall the action sequences twelve months later. [53][54]

To assess children and older adults Edit

Researchers use a variety of tasks to assess older children and adults' memory. Some examples are:

  • Paired associate learning – when one learns to associate one specific word with another. For example, when given a word such as "safe" one must learn to say another specific word, such as "green". This is stimulus and response. [55][56]
  • Free recall – during this task a subject would be asked to study a list of words and then later they will be asked to recall or write down as many words that they can remember, similar to free response questions. [57] Earlier items are affected by retroactive interference (RI), which means the longer the list, the greater the interference, and the less likelihood that they are recalled. On the other hand, items that have been presented lastly suffer little RI, but suffer a great deal from proactive interference (PI), which means the longer the delay in recall, the more likely that the items will be lost. [58]
  • Cued recall – one is given a significant hints to help retrieve information that has been previously encoded into the person's memory typically this can involve a word relating to the information being asked to remember. [59] This is similar to fill in the blank assessments used in classrooms.
  • Recognition – subjects are asked to remember a list of words or pictures, after which point they are asked to identify the previously presented words or pictures from among a list of alternatives that were not presented in the original list. [60] This is similar to multiple choice assessments.
  • Detection paradigm – individuals are shown a number of objects and color samples during a certain period of time. They are then tested on their visual ability to remember as much as they can by looking at testers and pointing out whether the testers are similar to the sample, or if any change is present.
  • Savings method – compares the speed of originally learning to the speed of relearning it. The amount of time saved measures memory. [61]
  • Implicit-memory tasks – information is drawn from memory without conscious realization.
  • Transience – memories degrade with the passing of time. This occurs in the storage stage of memory, after the information has been stored and before it is retrieved. This can happen in sensory, short-term, and long-term storage. It follows a general pattern where the information is rapidly forgotten during the first couple of days or years, followed by small losses in later days or years.
  • Absent-mindedness – Memory failure due to the lack of attention. Attention plays a key role in storing information into long-term memory without proper attention, the information might not be stored, making it impossible to be retrieved later.

Brain areas involved in the neuroanatomy of memory such as the hippocampus, the amygdala, the striatum, or the mammillary bodies are thought to be involved in specific types of memory. For example, the hippocampus is believed to be involved in spatial learning and declarative learning, while the amygdala is thought to be involved in emotional memory. [62]

Damage to certain areas in patients and animal models and subsequent memory deficits is a primary source of information. However, rather than implicating a specific area, it could be that damage to adjacent areas, or to a pathway traveling through the area is actually responsible for the observed deficit. Further, it is not sufficient to describe memory, and its counterpart, learning, as solely dependent on specific brain regions. Learning and memory are usually attributed to changes in neuronal synapses, thought to be mediated by long-term potentiation and long-term depression.

In general, the more emotionally charged an event or experience is, the better it is remembered this phenomenon is known as the memory enhancement effect. Patients with amygdala damage, however, do not show a memory enhancement effect. [63] [64]

Hebb distinguished between short-term and long-term memory. He postulated that any memory that stayed in short-term storage for a long enough time would be consolidated into a long-term memory. Later research showed this to be false. Research has shown that direct injections of cortisol or epinephrine help the storage of recent experiences. This is also true for stimulation of the amygdala. This proves that excitement enhances memory by the stimulation of hormones that affect the amygdala. Excessive or prolonged stress (with prolonged cortisol) may hurt memory storage. Patients with amygdalar damage are no more likely to remember emotionally charged words than nonemotionally charged ones. The hippocampus is important for explicit memory. The hippocampus is also important for memory consolidation. The hippocampus receives input from different parts of the cortex and sends its output out to different parts of the brain also. The input comes from secondary and tertiary sensory areas that have processed the information a lot already. Hippocampal damage may also cause memory loss and problems with memory storage. [65] This memory loss includes retrograde amnesia which is the loss of memory for events that occurred shortly before the time of brain damage. [61]

Cognitive neuroscientists consider memory as the retention, reactivation, and reconstruction of the experience-independent internal representation. The term of internal representation implies that such a definition of memory contains two components: the expression of memory at the behavioral or conscious level, and the underpinning physical neural changes (Dudai 2007). The latter component is also called engram or memory traces (Semon 1904). Some neuroscientists and psychologists mistakenly equate the concept of engram and memory, broadly conceiving all persisting after-effects of experiences as memory others argue against this notion that memory does not exist until it is revealed in behavior or thought (Moscovitch 2007).

One question that is crucial in cognitive neuroscience is how information and mental experiences are coded and represented in the brain. Scientists have gained much knowledge about the neuronal codes from the studies of plasticity, but most of such research has been focused on simple learning in simple neuronal circuits it is considerably less clear about the neuronal changes involved in more complex examples of memory, particularly declarative memory that requires the storage of facts and events (Byrne 2007). Convergence-divergence zones might be the neural networks where memories are stored and retrieved. Considering that there are several kinds of memory, depending on types of represented knowledge, underlying mechanisms, processes functions and modes of acquisition, it is likely that different brain areas support different memory systems and that they are in mutual relationships in neuronal networks: "components of memory representation are distributed widely across different parts of the brain as mediated by multiple neocortical circuits". [66]

    . Encoding of working memory involves the spiking of individual neurons induced by sensory input, which persists even after the sensory input disappears (Jensen and Lisman 2005 Fransen et al. 2002). Encoding of episodic memory involves persistent changes in molecular structures that alter synaptic transmission between neurons. Examples of such structural changes include long-term potentiation (LTP) or spike-timing-dependent plasticity (STDP). The persistent spiking in working memory can enhance the synaptic and cellular changes in the encoding of episodic memory (Jensen and Lisman 2005).
  • Working memory. Recent functional imaging studies detected working memory signals in both medial temporal lobe (MTL), a brain area strongly associated with long-term memory, and prefrontal cortex (Ranganath et al. 2005), suggesting a strong relationship between working memory and long-term memory. However, the substantially more working memory signals seen in the prefrontal lobe suggest that this area play a more important role in working memory than MTL (Suzuki 2007). and reconsolidation. Short-term memory (STM) is temporary and subject to disruption, while long-term memory (LTM), once consolidated, is persistent and stable. Consolidation of STM into LTM at the molecular level presumably involves two processes: synaptic consolidation and system consolidation. The former involves a protein synthesis process in the medial temporal lobe (MTL), whereas the latter transforms the MTL-dependent memory into an MTL-independent memory over months to years (Ledoux 2007). In recent years, such traditional consolidation dogma has been re-evaluated as a result of the studies on reconsolidation. These studies showed that prevention after retrieval affects subsequent retrieval of the memory (Sara 2000). New studies have shown that post-retrieval treatment with protein synthesis inhibitors and many other compounds can lead to an amnestic state (Nadel et al. 2000b Alberini 2005 Dudai 2006). These findings on reconsolidation fit with the behavioral evidence that retrieved memory is not a carbon copy of the initial experiences, and memories are updated during retrieval.

Study of the genetics of human memory is in its infancy though many genes have been investigated for their association to memory in humans and non-human animals. A notable initial success was the association of APOE with memory dysfunction in Alzheimer's disease. The search for genes associated with normally varying memory continues. One of the first candidates for normal variation in memory is the protein KIBRA, [67] which appears to be associated with the rate at which material is forgotten over a delay period. There has been some evidence that memories are stored in the nucleus of neurons. [68] [ non-primary source needed ]

Genetic underpinnings Edit

Several genes, proteins and enzymes have been extensively researched for their association with memory. Long-term memory, unlike short-term memory, is dependent upon the synthesis of new proteins. [69] This occurs within the cellular body, and concerns the particular transmitters, receptors, and new synapse pathways that reinforce the communicative strength between neurons. The production of new proteins devoted to synapse reinforcement is triggered after the release of certain signaling substances (such as calcium within hippocampal neurons) in the cell. In the case of hippocampal cells, this release is dependent upon the expulsion of magnesium (a binding molecule) that is expelled after significant and repetitive synaptic signaling. The temporary expulsion of magnesium frees NMDA receptors to release calcium in the cell, a signal that leads to gene transcription and the construction of reinforcing proteins. [70] For more information, see long-term potentiation (LTP).

One of the newly synthesized proteins in LTP is also critical for maintaining long-term memory. This protein is an autonomously active form of the enzyme protein kinase C (PKC), known as PKMζ. PKMζ maintains the activity-dependent enhancement of synaptic strength and inhibiting PKMζ erases established long-term memories, without affecting short-term memory or, once the inhibitor is eliminated, the ability to encode and store new long-term memories is restored. Also, BDNF is important for the persistence of long-term memories. [71]

The long-term stabilization of synaptic changes is also determined by a parallel increase of pre- and postsynaptic structures such as axonal bouton, dendritic spine and postsynaptic density. [72] On the molecular level, an increase of the postsynaptic scaffolding proteins PSD-95 and HOMER1c has been shown to correlate with the stabilization of synaptic enlargement. [72] The cAMP response element-binding protein (CREB) is a transcription factor which is believed to be important in consolidating short-term to long-term memories, and which is believed to be downregulated in Alzheimer's disease. [73]

DNA methylation and demethylation Edit

Rats exposed to an intense learning event may retain a life-long memory of the event, even after a single training session. The long-term memory of such an event appears to be initially stored in the hippocampus, but this storage is transient. Much of the long-term storage of the memory seems to take place in the anterior cingulate cortex. [74] When such an exposure was experimentally applied, more than 5,000 differently methylated DNA regions appeared in the hippocampus neuronal genome of the rats at one and at 24 hours after training. [75] These alterations in methylation pattern occurred at many genes that were down-regulated, often due to the formation of new 5-methylcytosine sites in CpG rich regions of the genome. Furthermore, many other genes were upregulated, likely often due to hypomethylation. Hypomethylation often results from the removal of methyl groups from previously existing 5-methylcytosines in DNA. Demethylation is carried out by several proteins acting in concert, including the TET enzymes as well as enzymes of the DNA base excision repair pathway (see Epigenetics in learning and memory). The pattern of induced and repressed genes in brain neurons subsequent to an intense learning event likely provides the molecular basis for a long-term memory of the event.

Epigenetics Edit

Studies of the molecular basis for memory formation indicate that epigenetic mechanisms operating in brain neurons play a central role in determining this capability. Key epigenetic mechanisms involved in memory include the methylation and demethylation of neuronal DNA, as well as modifications of histone proteins including methylations, acetylations and deacetylations.

Stimulation of brain activity in memory formation is often accompanied by the generation of damage in neuronal DNA that is followed by repair associated with persistent epigenetic alterations. In particular the DNA repair processes of non-homologous end joining and base excision repair are employed in memory formation. [ citation needed ]

Up until the mid-1980s it was assumed that infants could not encode, retain, and retrieve information. [76] A growing body of research now indicates that infants as young as 6-months can recall information after a 24-hour delay. [77] Furthermore, research has revealed that as infants grow older they can store information for longer periods of time 6-month-olds can recall information after a 24-hour period, 9-month-olds after up to five weeks, and 20-month-olds after as long as twelve months. [78] In addition, studies have shown that with age, infants can store information faster. Whereas 14-month-olds can recall a three-step sequence after being exposed to it once, 6-month-olds need approximately six exposures in order to be able to remember it. [52] [77]

Although 6-month-olds can recall information over the short-term, they have difficulty recalling the temporal order of information. It is only by 9 months of age that infants can recall the actions of a two-step sequence in the correct temporal order – that is, recalling step 1 and then step 2. [79] [80] In other words, when asked to imitate a two-step action sequence (such as putting a toy car in the base and pushing in the plunger to make the toy roll to the other end), 9-month-olds tend to imitate the actions of the sequence in the correct order (step 1 and then step 2). Younger infants (6-month-olds) can only recall one step of a two-step sequence. [77] Researchers have suggested that these age differences are probably due to the fact that the dentate gyrus of the hippocampus and the frontal components of the neural network are not fully developed at the age of 6-months. [53] [81] [82]

In fact, the term 'infantile amnesia' refers to the phenomenon of accelerated forgetting during infancy. Importantly, infantile amnesia is not unique to humans, and preclinical research (using rodent models) provides insight into the precise neurobiology of this phenomenon. A review of the literature from behavioral neuroscientist Dr Jee Hyun Kim suggests that accelerated forgetting during early life is at least partly due to rapid growth of the brain during this period. [83]

One of the key concerns of older adults is the experience of memory loss, especially as it is one of the hallmark symptoms of Alzheimer's disease. However, memory loss is qualitatively different in normal aging from the kind of memory loss associated with a diagnosis of Alzheimer's (Budson & Price, 2005). Research has revealed that individuals' performance on memory tasks that rely on frontal regions declines with age. Older adults tend to exhibit deficits on tasks that involve knowing the temporal order in which they learned information [84] source memory tasks that require them to remember the specific circumstances or context in which they learned information [85] and prospective memory tasks that involve remembering to perform an act at a future time. Older adults can manage their problems with prospective memory by using appointment books, for example.

Gene transcription profiles were determined for the human frontal cortex of individuals from age 26 to 106 years. Numerous genes were identified with reduced expression after age 40, and especially after age 70. [86] Genes that play central roles in memory and learning were among those showing the most significant reduction with age. There was also a marked increase in DNA damage, likely oxidative damage, in the promoters of those genes with reduced expression. It was suggested that DNA damage may reduce the expression of selectively vulnerable genes involved in memory and learning. [86]

Much of the current knowledge of memory has come from studying memory disorders, particularly amnesia. Loss of memory is known as amnesia. Amnesia can result from extensive damage to: (a) the regions of the medial temporal lobe, such as the hippocampus, dentate gyrus, subiculum, amygdala, the parahippocampal, entorhinal, and perirhinal cortices [87] or the (b) midline diencephalic region, specifically the dorsomedial nucleus of the thalamus and the mammillary bodies of the hypothalamus. [88] There are many sorts of amnesia, and by studying their different forms, it has become possible to observe apparent defects in individual sub-systems of the brain's memory systems, and thus hypothesize their function in the normally working brain. Other neurological disorders such as Alzheimer's disease and Parkinson's disease [89] can also affect memory and cognition. Hyperthymesia, or hyperthymesic syndrome, is a disorder that affects an individual's autobiographical memory, essentially meaning that they cannot forget small details that otherwise would not be stored. [90] Korsakoff's syndrome, also known as Korsakoff's psychosis, amnesic-confabulatory syndrome, is an organic brain disease that adversely affects memory by widespread loss or shrinkage of neurons within the prefrontal cortex. [61]

While not a disorder, a common temporary failure of word retrieval from memory is the tip-of-the-tongue phenomenon. Sufferers of Anomic aphasia (also called Nominal aphasia or Anomia), however, do experience the tip-of-the-tongue phenomenon on an ongoing basis due to damage to the frontal and parietal lobes of the brain.

Memory dysfunction can also occur after viral infections. [91] Many patients recovering from COVID-19 experience memory lapses. Other viruses can also elicit memory dysfunction, including SARS-CoV-1, MERS-CoV, Ebola virus and even influenza virus. [91] [92]

Interference can hamper memorization and retrieval. There is retroactive interference, when learning new information makes it harder to recall old information [93] and proactive interference, where prior learning disrupts recall of new information. Although interference can lead to forgetting, it is important to keep in mind that there are situations when old information can facilitate learning of new information. Knowing Latin, for instance, can help an individual learn a related language such as French – this phenomenon is known as positive transfer. [94]

Stress has a significant effect on memory formation and learning. In response to stressful situations, the brain releases hormones and neurotransmitters (ex. glucocorticoids and catecholamines) which affect memory encoding processes in the hippocampus. Behavioural research on animals shows that chronic stress produces adrenal hormones which impact the hippocampal structure in the brains of rats. [95] An experimental study by German cognitive psychologists L. Schwabe and O. Wolf demonstrates how learning under stress also decreases memory recall in humans. [96] In this study, 48 healthy female and male university students participated in either a stress test or a control group. Those randomly assigned to the stress test group had a hand immersed in ice cold water (the reputable SECPT or 'Socially Evaluated Cold Pressor Test') for up to three minutes, while being monitored and videotaped. Both the stress and control groups were then presented with 32 words to memorize. Twenty-four hours later, both groups were tested to see how many words they could remember (free recall) as well as how many they could recognize from a larger list of words (recognition performance). The results showed a clear impairment of memory performance in the stress test group, who recalled 30% fewer words than the control group. The researchers suggest that stress experienced during learning distracts people by diverting their attention during the memory encoding process.

However, memory performance can be enhanced when material is linked to the learning context, even when learning occurs under stress. A separate study by cognitive psychologists Schwabe and Wolf shows that when retention testing is done in a context similar to or congruent with the original learning task (i.e., in the same room), memory impairment and the detrimental effects of stress on learning can be attenuated. [97] Seventy-two healthy female and male university students, randomly assigned to the SECPT stress test or to a control group, were asked to remember the locations of 15 pairs of picture cards – a computerized version of the card game "Concentration" or "Memory". The room in which the experiment took place was infused with the scent of vanilla, as odour is a strong cue for memory. Retention testing took place the following day, either in the same room with the vanilla scent again present, or in a different room without the fragrance. The memory performance of subjects who experienced stress during the object-location task decreased significantly when they were tested in an unfamiliar room without the vanilla scent (an incongruent context) however, the memory performance of stressed subjects showed no impairment when they were tested in the original room with the vanilla scent (a congruent context). All participants in the experiment, both stressed and unstressed, performed faster when the learning and retrieval contexts were similar. [98]

This research on the effects of stress on memory may have practical implications for education, for eyewitness testimony and for psychotherapy: students may perform better when tested in their regular classroom rather than an exam room, eyewitnesses may recall details better at the scene of an event than in a courtroom, and persons suffering from post-traumatic stress may improve when helped to situate their memories of a traumatic event in an appropriate context.

Stressful life experiences may be a cause of memory loss as a person ages. Glucocorticoids that are released during stress, damage neurons that are located in the hippocampal region of the brain. Therefore, the more stressful situations that someone encounters, the more susceptible they are to memory loss later on. The CA1 neurons found in the hippocampus are destroyed due to glucocorticoids decreasing the release of glucose and the reuptake of glutamate. This high level of extracellular glutamate allows calcium to enter NMDA receptors which in return kills neurons. Stressful life experiences can also cause repression of memories where a person moves an unbearable memory to the unconscious mind. [61] This directly relates to traumatic events in one's past such as kidnappings, being prisoners of war or sexual abuse as a child.

The more long term the exposure to stress is, the more impact it may have. However, short term exposure to stress also causes impairment in memory by interfering with the function of the hippocampus. Research shows that subjects placed in a stressful situation for a short amount of time still have blood glucocorticoid levels that have increased drastically when measured after the exposure is completed. When subjects are asked to complete a learning task after short term exposure they often have difficulties. Prenatal stress also hinders the ability to learn and memorize by disrupting the development of the hippocampus and can lead to unestablished long term potentiation in the offspring of severely stressed parents. Although the stress is applied prenatally, the offspring show increased levels of glucocorticoids when they are subjected to stress later on in life. [99] One explanation for why children from lower socioeconomic backgrounds tend to display poorer memory performance than their higher-income peers is the effects of stress accumulated over the course of the lifetime. [100] The effects of low income on the developing hippocampus is also thought be mediated by chronic stress responses which may explain why children from lower and higher-income backgrounds differ in terms of memory performance. [101]

Making memories occurs through a three-step process, which can be enhanced by sleep. The three steps are as follows:

Sleep affects memory consolidation. During sleep, the neural connections in the brain are strengthened. This enhances the brain's abilities to stabilize and retain memories. There have been several studies which show that sleep improves the retention of memory, as memories are enhanced through active consolidation. System consolidation takes place during slow-wave sleep (SWS). [102] This process implicates that memories are reactivated during sleep, but that the process doesn't enhance every memory. It also implicates that qualitative changes are made to the memories when they are transferred to long-term store during sleep. During sleep, the hippocampus replays the events of the day for the neocortex. The neocortex then reviews and processes memories, which moves them into long-term memory. When one does not get enough sleep it makes it more difficult to learn as these neural connections are not as strong, resulting in a lower retention rate of memories. Sleep deprivation makes it harder to focus, resulting in inefficient learning. [102] Furthermore, some studies have shown that sleep deprivation can lead to false memories as the memories are not properly transferred to long-term memory. One of the primary functions of sleep is thought to be the improvement of the consolidation of information, as several studies have demonstrated that memory depends on getting sufficient sleep between training and test. [103] Additionally, data obtained from neuroimaging studies have shown activation patterns in the sleeping brain that mirror those recorded during the learning of tasks from the previous day, [103] suggesting that new memories may be solidified through such rehearsal. [104]

Although people often think that memory operates like recording equipment, this is not the case. The molecular mechanisms underlying the induction and maintenance of memory are very dynamic and comprise distinct phases covering a time window from seconds to even a lifetime. [105] In fact, research has revealed that our memories are constructed: "current hypotheses suggest that constructive processes allow individuals to simulate and imagine future episodes, [106] happenings, and scenarios. Since the future is not an exact repetition of the past, simulation of future episodes requires a complex system that can draw on the past in a manner that flexibly extracts and recombines elements of previous experiences – a constructive rather than a reproductive system." [66] People can construct their memories when they encode them and/or when they recall them. To illustrate, consider a classic study conducted by Elizabeth Loftus and John Palmer (1974) [107] in which people were instructed to watch a film of a traffic accident and then asked about what they saw. The researchers found that the people who were asked, "How fast were the cars going when they smashed into each other?" gave higher estimates than those who were asked, "How fast were the cars going when they hit each other?" Furthermore, when asked a week later whether they had seen broken glass in the film, those who had been asked the question with smashed were twice more likely to report that they had seen broken glass than those who had been asked the question with hit. There was no broken glass depicted in the film. Thus, the wording of the questions distorted viewers' memories of the event. Importantly, the wording of the question led people to construct different memories of the event – those who were asked the question with smashed recalled a more serious car accident than they had actually seen. The findings of this experiment were replicated around the world, and researchers consistently demonstrated that when people were provided with misleading information they tended to misremember, a phenomenon known as the misinformation effect. [108]

Research has revealed that asking individuals to repeatedly imagine actions that they have never performed or events that they have never experienced could result in false memories. For instance, Goff and Roediger [109] (1998) asked participants to imagine that they performed an act (e.g., break a toothpick) and then later asked them whether they had done such a thing. Findings revealed that those participants who repeatedly imagined performing such an act were more likely to think that they had actually performed that act during the first session of the experiment. Similarly, Garry and her colleagues (1996) [110] asked college students to report how certain they were that they experienced a number of events as children (e.g., broke a window with their hand) and then two weeks later asked them to imagine four of those events. The researchers found that one-fourth of the students asked to imagine the four events reported that they had actually experienced such events as children. That is, when asked to imagine the events they were more confident that they experienced the events.

Research reported in 2013 revealed that it is possible to artificially stimulate prior memories and artificially implant false memories in mice. Using optogenetics, a team of RIKEN-MIT scientists caused the mice to incorrectly associate a benign environment with a prior unpleasant experience from different surroundings. Some scientists believe that the study may have implications in studying false memory formation in humans, and in treating PTSD and schizophrenia. [111] [112]

Memory reconsolidation is when previously consolidated memories are recalled or retrieved from long-term memory to your active consciousness. During this process, memories can be further strengthened and added to but there is also risk of manipulation involved. We like to think of our memories as something stable and constant when they are stored in long-term memory but this isn't the case. There are a large number of studies that found that consolidation of memories is not a singular event but are put through the process again, known as reconsolidation. [113] This is when a memory is recalled or retrieved and placed back into your working memory. The memory is now open to manipulation from outside sources and the misinformation effect which could be due to misattributing the source of the inconsistent information, with or without an intact original memory trace (Lindsay and Johnson, 1989). [114] One thing that can be sure is that memory is malleable.

This new research into the concept of reconsolidation has opened the door to methods to help those with unpleasant memories or those that struggle with memories. An example of this is if you had a truly frightening experience and recall that memory in a less arousing environment, the memory will be weaken the next time it is retrieved. [113] "Some studies suggest that over-trained or strongly reinforced memories do not undergo reconsolidation if reactivated the first few days after training, but do become sensitive to reconsolidation interference with time." [113] This, however does not mean that all memory is susceptible to reconsolidation. There is evidence to suggest that memory that has undergone strong training and whether or not is it intentional is less likely to undergo reconsolidation. [115] There was further testing done with rats and mazes that showed that reactivated memories were more susceptible to manipulation, in both good and bad ways, than newly formed memories. [116] It is still not known whether or not these are new memories formed and it's an inability to retrieve the proper one for the situation or if it's a reconsolidated memory. Because the study of reconsolidation is still a newer concept, there is still debate on whether it should be considered scientifically sound.

A UCLA research study published in the June 2008 issue of the American Journal of Geriatric Psychiatry found that people can improve cognitive function and brain efficiency through simple lifestyle changes such as incorporating memory exercises, healthy eating, physical fitness and stress reduction into their daily lives. This study examined 17 subjects, (average age 53) with normal memory performance. Eight subjects were asked to follow a "brain healthy" diet, relaxation, physical, and mental exercise (brain teasers and verbal memory training techniques). After 14 days, they showed greater word fluency (not memory) compared to their baseline performance. No long-term follow-up was conducted it is therefore unclear if this intervention has lasting effects on memory. [117]

There are a loosely associated group of mnemonic principles and techniques that can be used to vastly improve memory known as the art of memory.

The International Longevity Center released in 2001 a report [118] which includes in pages 14–16 recommendations for keeping the mind in good functionality until advanced age. Some of the recommendations are to stay intellectually active through learning, training or reading, to keep physically active so to promote blood circulation to the brain, to socialize, to reduce stress, to keep sleep time regular, to avoid depression or emotional instability and to observe good nutrition.

Memorization is a method of learning that allows an individual to recall information verbatim. Rote learning is the method most often used. Methods of memorizing things have been the subject of much discussion over the years with some writers, such as Cosmos Rossellius using visual alphabets. The spacing effect shows that an individual is more likely to remember a list of items when rehearsal is spaced over an extended period of time. In contrast to this is cramming: an intensive memorization in a short period of time. the spacing effect is exploited to improve memory in spaced repetition flashcard training. Also relevant is the Zeigarnik effect which states that people remember uncompleted or interrupted tasks better than completed ones. The so-called Method of loci uses spatial memory to memorize non-spatial information. [119]

Plants lack a specialized organ devoted to memory retention, so plant memory has been a controversial topic in recent years. New advances in the field have identified the presence of neurotransmitters in plants, adding to the hypothesis that plants are capable of remembering. [120] Action potentials, a physiological response characteristic of neurons, have been shown to have an influence on plants as well, including in wound responses and photosynthesis. [120] In addition to these homologous features of memory systems in both plants and animals, plants have also been observed to encode, store and retrieve basic short-term memories.

One of the most well-studied plants to show rudimentary memory is the Venus flytrap. Native to the subtropical wetlands of the eastern United States, Venus Fly Traps have evolved the ability to obtain meat for sustenance, likely due to the lack of nitrogen in the soil. [121] This is done by two trap-forming leaf tips that snap shut once triggered by a potential prey. On each lobe, three triggers hairs await stimulation. In order to maximize the benefit to cost ratio, the plant enables a rudimentary form of memory in which two trigger hairs must be stimulated within 30 seconds in order to result in trap closure. [121] This system ensures that the trap only closes when potential prey is within grasp.

The time lapse between trigger hair stimulations suggests that the plant can remember an initial stimulus long enough for a second stimulus to initiate trap closure. This memory isn't encoded in a brain, as plants lack this specialized organ. Rather, information is stored in the form of cytoplasmic calcium levels. The first trigger causes a subthreshold cytoplasmic calcium influx. [121] This initial trigger isn't enough to activate trap closure, so a subsequent stimulus allows for a secondary influx of calcium. The latter calcium rise superimposes on the initial one, creating an action potential that passes threshold, resulting in trap closure. [121] Researchers, to prove that an electrical threshold must be met to stimulate trap closure, excited a single trigger hair with a constant mechanical stimulus using Ag/AgCl electrodes. [122] The trap closed after only a few seconds. This experiment gave evidence to demonstrate that the electrical threshold, not necessarily the number of trigger hair stimulations, was the contributing factor in Venus Fly Trap memory. It has been shown that trap closure can be blocked using uncouplers and inhibitors of voltage-gated channels. [122] After trap closure, these electrical signals stimulate glandular production of jasmonic acid and hydrolases, allowing for digestion of the prey. [123]

The field of plant neurobiology has gained a large amount of interest over the past decade, leading to an influx of research regarding plant memory. Although the Venus flytrap is one of the more highly studied, many other plants exhibit the capacity to remember, including the Mimosa pudica through an experiment conducted by Monica Gagliano and colleagues in 2013. [124] To study the Mimosa pudica, Gagliano designed an appartus with which potted mimosa plants could be repeatedly dropped the same distance and at the same speed. It was observed that the plants defensive response of curling up its leaves decreased over the 60 times the experiment was repeated per plant. To confirm that this was a mechanism of memory rather than exhaustion, some of the plants were shaken post experiment and displayed normal defensive responses of leaf curling. This experiment also demonstrated long term memory in the plants, as it was repeated a month later and the plants were observed to remain unfazed by the dropping. As the field expands, it is likely that we will learn more about the capacity of a plant to remember.

HM, the Man with No Memory

Henry Molaison, known by thousands of psychology students as "HM," lost his memory on an operating table in a hospital in Hartford in August 1953. He was 27 years old and had suffered from epileptic seizures for many years.

William Beecher Scoville, a Hartford neurosurgeon, stood above an awake Henry and skilfully suctioned out the seahorse-shaped brain structure called the hippocampus that lay within each temporal lobe. Henry would have been drowsy and probably didn't notice his memory vanishing as the operation proceeded.

The operation was successful in that it significantly reduced Henry's seizures, but it left him with a dense memory loss. When Scoville realized his patient had become amnesic, he referred him to the eminent neurosurgeon Dr. Wilder Penfield and neuropsychologist Dr. Brenda Milner of Montreal Neurological Institute (MNI), who assessed him in detail. Up until then, it had not been known that the hippocampus was essential for making memories, and that if we lose both of them we will suffer a global amnesia. Once this was realized, the findings were widely publicized so that this operation to remove both hippocampi would never be done again.

Penfield and Milner had already been conducting memory experiments on other patients and they quickly realized that Henry's dense amnesia, his intact intelligence, and the precise neurosurgical lesions made him the perfect experimental subject. For 55 years, Henry participated in numerous experiments, primarily at Massachusetts Institute of Technology (MIT), where Professor Suzanne Corkin and her team of neuropsychologists assessed him.

Access to Henry was carefully restricted to less than 100 researchers (I was honored to be one of them), but the MNI and MIT studies on HM taught us much of what we know about memory. Of course, many other patients with memory impairments have since been studied, including a small number with amnesias almost as dense as Henry's, but it is to him we owe the greatest debt. His name (or initials!) has been mentioned in almost 12,000 journal articles, making him the most studied case in medical or psychological history. Henry died on December 2, 2008, at the age of 82. Until then, he was known to the world only as "HM," but on his death his name was revealed. A man with no memory is vulnerable, and his initials had been used while he lived in order to protect his identity.

Henry's memory loss was far from simple. Not only could he make no new conscious memories after his operation, he also suffered a retrograde memory loss (a loss of memories prior to brain damage) for an 11-year period before his surgery. It is not clear why this is so, although it is thought this is not because of his loss of the hippocampi on both sides of his brain. More likely it is a combination of his being on large doses of antiepileptic drugs and his frequent seizures prior to his surgery. His global amnesia for new material was the result of the loss of both hippocampi, and meant that he could not learn new words, songs or faces after his surgery, forgot who he was talking to as soon as he turned away, didn't know how old he was or if his parents were alive or dead, and never again clearly remembered an event, such as his birthday party, or who the current president of the United States was.

In contrast, he did retain the ability to learn some new motor skills, such as becoming faster at drawing a path through a picture of a maze, or learning to use a walking frame when he sprained his ankle, but this learning was at a subconscious level. He had no conscious memory that he had ever seen or done the maze test before, or used the walking frame previously.

We measure time by our memories, and thus for Henry, it was as if time stopped when he was 16 years old, 11 years before his surgery. Because his intelligence in other non-memory areas remained normal, he was an excellent experimental participant. He was also a very happy and friendly person and always a delight to be with and to assess. He never seemed to get tired of doing what most people would think of as tedious memory tests, because they were always new to him! When he was at MIT, between test sessions he would often sit doing crossword puzzles, and he could do the same ones again and again if the words were erased, as to him it was new each time.

Henry gave science the ultimate gift: his memory. Thousands of people who have suffered brain damage, whether through accident, disease or a genetic quirk, have given similar gifts to science by agreeing to participate in psychological, neuropsychological, psychiatric and medical studies and experiments, and in some cases by gifting their brains to science after their deaths. Our knowledge of brain disease and how the normal mind works would be greatly diminished if it were not for the generosity of these people and their families (who are frequently also involved in interviews, as well as transporting the "patient" back and forth to the psychology laboratory). After Henry's death, his brain was dissected into 2,000 slices and digitized as a three-dimensional brain map that could be searched by zooming in from the whole brain to individual neurons. Thus, his tragically unique brain has been preserved for posterity.

The types of amnesia

To understand how we remember things, it's incredibly helpful to study how we forget—which is why neuroscientists study amnesia, the loss of memories or the ability to learn. Amnesia is usually the result of some kind of trauma to the brain, such as a head injury, a stroke, a brain tumor, or chronic alcoholism.

There are two main types of amnesia. The first, retrograde amnesia, occurs where you forget things you knew before the brain trauma. Anterograde amnesia is when brain trauma curtails or stops someone's ability to form new memories.

The most famous case study of anterograde amnesia is Henry Molaison, who in 1953 had parts of his brain removed as a last-ditch treatment for severe seizures. While Molaison—known when he was alive as H.M.—remembered much of his childhood, he was unable to form new declarative memories. People who worked with him for decades had to re-introduce themselves with every visit.

By studying people such as H.M., as well as animals with different types of brain damage, scientists can trace where and how different kinds of memories form in the brain. It seems that short-term and long-term memories don't form in exactly the same way, nor do declarative and procedural memories.

There's no one place within the brain that holds all of your memories different areas of the brain form and store different kinds of memories, and different processes may be at play for each. For instance, emotional responses such as fear reside in a brain region called the amygdala. Memories of the skills you've learned are associated with a different region called the striatum. A region called the hippocampus is crucial for forming, retaining, and recalling declarative memories. The temporal lobes, the brain regions that H.M. was partially missing, play a crucial role in forming and recalling memories.

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How to remove an RFID IMPLANT

Written by The Truth Denied, , 419 Comments

* This image (above) is from a French documentary showing a VeriChip being surgically removed from the arm of a journalist. Source: News of the world – RFID

2017 Updates : Popular Science put an article out called ‘Why Did I Implant A Chip In My Hand?’ that most of you may want to read. Please look at the size of the chip, and as you are looking over your own body, can you tell us how large or small your chip is, where ever it’s location may be on your body?

Please be sure to visit the comment section when you are finished reading the article for advice from other TI’s.

RFID technology could lead to political repression as governments could use implants to track and target human rights activists, labor activists, civil dissidents, and political opponents criminals and domestic abusers could use them to stalk and harass their victims slaveholders could use them to prevent captives from escaping and child abusers could use them to locate and abduct children. So what do we do about this?

Most of the TI’s that I have spoken have similar concerns when it comes to implant devices the removal of an RFID implant is complicated whether you are a pet or a human. First you have to find a practitioner who can detect the chip.This is usually not so easy to do as some of the chips do not show up on X-rays, ultrasound machines, or scanners.Once you have successfully determined that you do have an implant ,you better hope the chip stays in one location, 90% of the time they tend to move around the body. Secondly, you must find a surgeon who is willing to remove the chip, or find a technician who can erase the chip and stop it from transmitting data. The following is sure to help those of you who may have strong implications of chip implantation. This article is to aid you in your search for either chip detection and or chip removal.

What is an RFID (Radio Frequency Identification) implant?

RFID is a technology for identifying unique medical equipment and supplies and other high value assets using radio waves. Typical RFID systems are made up of two major components: Readers and Tags. RFID tags are also referred to as a ‘chip’. RFID stands for Radio Frequency Identification.

The RFID reader (also called a scanner), is set to a particular electromagnetic frequency, and an RFID tag, which consists of a microchip is connected to an antenna. The microchip contains information that is transmitted to the scanner when the chip is within its range. The chips are generally the size of a grain of rice, but more recent technology is smaller. Uses for the RFID Chip include tracking for pets, medical patient data and records, military recruits,credit & debit cards cards, US Dollar, consumer goods, and even livestock. You name it, it’s got a chip.

The RFID labels draw their power from the reader. The reader transmits a low power radio signal through its antenna to the tag. The tag receives it through its own antenna to power the integrated circuit (micro-chip) that is built-into the label. The tag will briefly communicate with the reader for verification that the tag was “read” and data is exchanged. RFID systems were originally developed created as an alternative to barcodes, so they say. If you are not familiar with RFID technology yet, I would suggest that you begin to at least familiarizing yourself with it, mainly because the number of different devices that utilize these types of tags is growing exponentially. The main reason someone would want to block or destroy RFID chips would be to maintain privacy.

How did you get your implant if you never authorized it?

It is becoming more and more obvious that almost all of us have been implanted with chips in one way or another since we were born, but how? And exactly WHO is doing the implants?

Vaccinations, flu shots, dental work, surgeries, sleep abductions, in fact most medicine including dentistry has been loaded with implantable chips since the 1960s. They have had this technology for 40 years or more and are just now bringing it out to condition and introduce it to the public. Withholding technology is typical for the government and military for years before they release it to the public for whatever reason. Most of the time new technologies have been beneficial, but implantable chips are not one of them. If you wish to further your knowledge on current technology regarding frequency and reading distances of the RFID CHIP, we have provided a manual from DEFCON:

Removal of an RFID Implant: Now that you have one, how do you get rid of it?

“The implantable microchip can be removed from the body – but it’s not like removing a splinter. This image is from a French documentary showing a VeriChip being surgically removed from the arm of a journalist. Source: News of the world – RFID CNN reporter Robyn Curnow confirms that chip removal is difficult. She was implanted with a VeriChip in a Spanish night club in 2004 and had the device removed later that year. She reports that the surgery was a challenge for the doctors involved, a far cry from “removing a splinter.” Here is her report: Once back home in London, I begin to feel uncomfortable and unsure about my microchip implant. The Baja Beach Club Web site assures that getting rid of the microchip is a simple and harmless procedure, something like removing a splinter. But the two doctors I consulted in London’s Harley Street disagreed. Getting the microchip removed became serious business.”

The following is from a reader who had an unbearable ringing in their ears and suspected they had an implant. This is an excerpt from part of their letter.

“That night, taking the advice on your website, 3/4″ Neodymium magnets were now placed on the top arch of the ear, one if front, and one behind. But the ear had been cut, and the force of the magnets became so painful, they were not able to sleep with them on more than 2 hours before having to remove them.”

Only days have gone by… but the sound has not returned. (Referring to the ringing and beeping noises.)”

Magnets can also be found inside old hard drives. They will be encased in a silver (or gold) overlay because they are more brittle than other magnets. But you will not mistake them, because the moment you try to put them together you will pinch your fingers. They are very powerful magnets, derived from a rare earth mineral.

And they WILL render micro-chips useless.” Original source

RFID REMOVAL: The photos clearly show something foreign that is not organic mixed with the biological tissue

The photos contained in this document are of micro stimulator devices that were surgically recovered and analyzed by using microscopy and by materials characterization techniques. The recovered devices are an exact match for the devices that were developed by research scientists Joseph Schulman, Gerald Loeb and Philip Troyk under contract from the National Institutes of Health. There are about 4 contracts involved, but the initial contract was #N01-NS5-2325 and funded by the NIH/NINDS/NPP. More information regarding these contracts can be found at the NIH Neural Prosthesis Project website. The following list briefly outlines some of the evidence presented in this document .AMAZING PDF and DOCUMENTATION of LARSON’s CHIP


Please check out this interview with James Walbert who is one of the Board of Directors for the Stalking Victims Network. James Walbert is a victim of non-consensual RFID implantation. He has testified in in Washington D.C. in front of the Presidential Commission on Bioethical issues appointed by President Obahma.He is one of the few who obtained a “Protection Order” for James Walbert.

When I asked James Walbert why he did not elect to have his implant removed, he stated “Because I don’t think it’s time”.

How to deactivate an RFID Chip/Implant

“I have found that rare earth magnets called Neodymium magnets will nullify chips. I bought some Neodymium magnets online from a retailer, the kind that can lift 10lbs of steel and run about .70 cents apiece and I used band aides to hold them in place. I put magnets on the back of each ear lobe, on the side of each arm where I have received shots, on both sides of my jaws where I had wisdom teeth removed, and under each heel where I had been purposely implanted by my mother’s doctor shortly after I was born. Also on my stomach where I had a cesarean. I am finding that most people are implanted by their navels as well. If you have had any type of surgery put a magnet near the scar for about 24 hours.”

“For the electronic, physical, (implants), neodymium (rare earth mineral) magnets of anywhere from a quarter inch to a half inch in diameter work very well to completely disable them. Some people wear them in the headband of a baseball cap, preferably for at least 24 hours, but you can also tape them to the back of your ear and hide them under your hair! After implants are disabled, you won’t have so much fatigue, and the pitch or frequency in your ear stops happening. Use caution with these powerful magnets, though, as they can wipe out disks and computers. It’s best not to wear them while sitting at the computer, at least, not while wearing more than one or two of the little ones.”

The following are comments of those who have tags and implants and these are excerpts from their discussions. They don’t seem to be bothered by having the implant, they chose the injection. They often refer to it as biohacking .

I have a 125kHz EM4102 tag in my left hand and have for almost two years.

I’ve been wondering if you think it’s worth it to remove my current tag and upgrade to a 13.56mHz S50. Is the read range about the same, worse, or greater? Really I love that you can use it with Android phones (even though I’m an iOS guy) and it seems slightly more future-proof for maybe another 5 years at least (total guess.) I’d have to replace two RFID readers however and re-inject myself which isn’t terrible- it just costs more. Any thoughts or alternatives? I get in my house and turn my lights on and off. (I’ve even thought about buying a bunch and putting them in my clothing!)”

You can have your 125kHz tag removed and replace it with an S50, but why not just put the S50 into the other hand? Of course range depends on a lot of factors like reader antenna shape and power output, but overall range is slightly less than the EM4102 if you’re talking about using a phone to read the tag. Here are a few videos you should check out

As for future-proofing, with over 150+ million access control systems around the world that use the EM42xx family of tags – I don’t think the EM4102 is going out of style any time soon. That’s why I’d suggest just getting the S50 put into the other hand rather than replacing the EM4102… then you’d simply have more options!” End Discussion

“We believe that Biohacking is the Forefront of a new kind of evolution.” Founder of the website Dangerous Things.

Talk about the new frontier!

About the Author

Roxy Lopez of The Truth Denied

Lopez has been reaching out to the public most of her adult life regarding many subject matters that revolve around government secrecies such as GMO’s, UFO Sightings, Morgellons Disease ,and Chemtrails, just to name a few. Lopez states that “The TRUTH has been DENIED us all, and in this current age of technology we now afford the right to access it once and for all.”

The Truth Denied acquired worldwide attention when Lopez made a global stance against Geoengineering (aka Chemtrails), GMO’s, Fracking , environmental health hazards, Morgellons Disease, Gang stalking and illegal government surveillance programs that are increasingly on the up rise. Roxy opens the can of worms to the secrets that the Global Government is keeping from us all.

Microwave frequency electromagnetic fields (EMFs) produce widespread neuropsychiatric effects including depression

Non-thermal microwave/lower frequency electromagnetic fields (EMFs) act via voltage-gated calcium channel (VGCC) activation. Calcium channel blockers block EMF effects and several types of additional evidence confirm this mechanism. Low intensity microwave EMFs have been proposed to produce neuropsychiatric effects, sometimes called microwave syndrome, and the focus of this review is whether these are indeed well documented and consistent with the known mechanism(s) of action of such EMFs. VGCCs occur in very high densities throughout the nervous system and have near universal roles in release of neurotransmitters and neuroendocrine hormones. Soviet and Western literature shows that much of the impact of non-thermal microwave exposures in experimental animals occurs in the brain and peripheral nervous system, such that nervous system histology and function show diverse and substantial changes. These may be generated through roles of VGCC activation, producing excessive neurotransmitter/neuroendocrine release as well as oxidative/nitrosative stress and other responses. Excessive VGCC activity has been shown from genetic polymorphism studies to have roles in producing neuropsychiatric changes in humans. Two U.S. government reports from the 1970s to 1980s provide evidence for many neuropsychiatric effects of non-thermal microwave EMFs, based on occupational exposure studies. 18 more recent epidemiological studies, provide substantial evidence that microwave EMFs from cell/mobile phone base stations, excessive cell/mobile phone usage and from wireless smart meters can each produce similar patterns of neuropsychiatric effects, with several of these studies showing clear dose-response relationships. Lesser evidence from 6 additional studies suggests that short wave, radio station, occupational and digital TV antenna exposures may produce similar neuropsychiatric effects. Among the more commonly reported changes are sleep disturbance/insomnia, headache, depression/depressive symptoms, fatigue/tiredness, dysesthesia, concentration/attention dysfunction, memory changes, dizziness, irritability, loss of appetite/body weight, restlessness/anxiety, nausea, skin burning/tingling/dermographism and EEG changes. In summary, then, the mechanism of action of microwave EMFs, the role of the VGCCs in the brain, the impact of non-thermal EMFs on the brain, extensive epidemiological studies performed over the past 50 years, and five criteria testing for causality, all collectively show that various non-thermal microwave EMF exposures produce diverse neuropsychiatric effects.

Keywords: Excessive calcium effects Low-intensity microwave electromagnetic fields Oxidative/nitrosative stress.

How 'Inside Out' Explains The Science Of Memory

Inside Out is not just Pixar's best film since Toy Story 3, it's also the smartest. Mostly set inside the mind of 11-year-old Riley as she moves to a new town, the movie uses colorful characters to illustrate how emotions influence our memories.

We humans have two main memory systems: implicit and explicit. Implicit memory includes unconscious processes like emotional and skeletal responses, learning skills and habits, plus reflex actions. Explicit memory stores facts and events, and recalling that information requires conscious awareness. The two systems can be separate, which is why you might retain an implicit fear of clowns after forgetting the explicit experience that originally triggered your coulrophobia. The two memory systems can also be connected when events have emotional significance – the focus of Pixar's film.

Outward emotions

Inside Out depicts five emotions as characters with distinct personalities: Joy, Fear, Disgust, Anger and Sadness. These are inspired by the work of American psychologist Robert Plutchik, who proposed that we have eight basic emotions, which can be arranged on a wheel with pairs of opposites: joy and sadness, anger and fear, trust and disgust, anticipation and surprise.

Robert Plutchik's wheel of emotions (Image: Wikipedia)

Plutchik called this idea a 'psycho-evolutionary synthesis' because it's based on Charles Darwin's theory that an animal's outward expressions reflect emotions that help them survive. As stated at the start of Inside Out, fear stops you from putting yourself in danger, for example, while disgust prevents you from poisoning yourself. Although the film's major characters are Joy and Sadness, the most vital emotion in nature is fear. Having emotions is driven by natural selection: if an animal isn't able to recognise a potential threat, it risks being killed.

Learning and memory helps animals respond quickly to situations that resemble past experiences, which improves its chances of survival. Attaching emotions to an event gives that explicit memory some context, and also makes it stronger. As Riley's imaginary friend Bing Bong says, "When Riley doesn't care about memories, they fade."

In Inside Out, each memory is a glowing orb whose colours match the movie's five emotions: yellow for joy, blue for sadness, red for anger, purple for fear, and green for disgust. Memories aren't limited to a single emotion, as shown at the end of the film when most of Riley's memory orbs aren't uniform, but become marbles filled with multicoloured swirls of emotions. For example, while not named in the movie, combining joy and sadness (blue and yellow) creates sentimental feelings for the past, or nostalgia (Greek for 'ache for home').

Inside the brain

So how do memories and emotions become connected? The process begins with stress hormones released by adrenal glands, which ultimately activate the amygdala, a pair of tonsil-sized areas in each brain hemisphere. The amygdala is located above a pair of seahorse-shaped structures called the hippocampus, which is roughly equivalent to Inside Out's aptly-named 'Headquarters'. The five emotions personify the amygdala, and attach emotional significance to a new memory by pressing a big button on the control console in Headquarters, which is akin to nerve cells (neurons) in the amygdala sending signals to the hippocampus.

Brain areas associated with emotional responses (Image CC BY 3.0: OpenStax College / . [+]

Memory has two lifespans: working (or 'short-term') and long-term. Working memory keeps knowledge in mind for cognitive functions like learning and reasoning, enabling us to compare and contrast information. Long-term memory is needed when the brain is presented with more information than it can handle, such as when you're asked to memorise 10 words at once.

Long-term storage of facts and events (explicit memory) depends on the hippocampus, as proven by the case of 'HM', who suffered from epileptic seizures. In their famous 1957 study, surgeon William Scoville and neuroscientist Brenda Milner removed a small part of HM's brain, the hippocampus and surrounding areas within the medial temporal lobe. The procedure cured HM of epilepsy, but also left the patient with anterograde amnesia – the inability to form new long-term memories.

Long-term memory in Inside Out (Image: Disney/Pixar)

The memory orbs of Inside Out are sent through vacuum tubes down to 'Long Term', a library of endless shelves that hold Riley's memories. From above, Long Term looks like the cerebral cortex, folded outer layers that make a mammal's brain to resemble a walnut. Jellybean-like characters known as 'Mind Workers' pick memories off a shelf and thrown them into the 'Memory Dump', a deep chasm where the unwanted orbs go dull and the information they carry – such as old phone numbers and piano lessons – is soon forgotten.

Scattered storage

In the movie, an individual memory is a single orb. But in the brain, each memory doesn't exist in a specific location, but as a branching network of neurons. More precisely, each memory is stored or 'encoded' as a pattern of synapses, as the tiny gaps between brain cells. (An adult brain has 86 billion neurons, each with about a thousand synapses.) The pattern of nerve impulses across the cerebral cortex creates the physical trace of a memory, what scientists call an 'engram'.

Sleep is an important process for learning and storing memories. The brain's hypothalamus – located above the amygdala – controls the switch between being awake or asleep. In Inside Out, Riley enters REM (rapid-eye movement) sleep the second she closes her eyes. In reality, we fall into non-REM first, then alternate between REM and non-REM over 4-5 sleep cycles during the night.

REM sleep often includes dreaming, and one theory for why we dream is that the sensations and emotions we experience are a side-effect of random firing of impulses during the strengthening and pruning of the connections between neuron branches. Our brain tries to make sense of our thoughts by stitching them together into a logical story. In Pixar's film, Riley's mind has a studio called 'Dream Production' that creates movies based on her past experiences. This often creates a disjointed narrative. As Fear shouts while watching a dream, "Boo! Pick a plot line!"

Unreliable recall

Your memory isn't as reliable as you might think. Research by American psychologist Elizabeth Loftus has shown that our minds can be manipulated via a 'misinformation effect' that implants false memories. In a 1974 study, Loftus showed participants a video of a car crash, then told them to recall the accident. After being asked a leading question or changing one minor detail, like using the word 'smashed' instead of 'hit', people would estimate that vehicles had travelled at faster speeds, and remembered seeing broken glass – even though it wasn't there. This highlights the dangers of relying on eyewitness testimony alone during criminal trials.

Memory recall in Inside Out (Image: Disney/Pixar)

In Inside Out, recall occurs when memory orbs from Long Term are sent back up to Headquarters, where a projector shines light through the orb so a past event is replayed on a screen in front of the control console. Although this is the most common way to show the past in the medium of moving pictures, it perpetuates the myth that individual memories are recorded as linear film sequences that we can rewind or fast-forward.

But in the brain, each memory actually consists of scattered information – synaptic connections between neurons – that only leave a physical trace during storage or recall. Every time a memory is accessed, its bits are pieced back together. And so instead of retrieval, it's more accurate to describe recall as 'recollection'. The process of converting information in working memory to long-term is known as 'consolidation', and scientists have found that recall can sometimes cause memories to be reconsolidated. This means there's potential for a memory to become modified by synapses that weren't part of its original physical trace.

Inside Out also shows that the association between explicit events and implicit emotions isn't permanent, as illustrated whenever the character Sadness changes a memory orb's colour from yellow (joy) to blue. Researchers are testing ways to exploit reconsolidation to improve mental health. Drugs like propranolol (a beta blocker that interferes with molecules that help form and maintain memories) can be given while someone relives a bad experience to cut synaptic connections between an event and its associated emotions. This could reduce the emotional impact of flashbacks that soldiers experience in post-traumatic stress disorder (PTSD), for example.

The unreliable nature of human memory is illustrated at the end of Inside Out, when Joy realises that one of Riley's happiest moments followed an unhappy event, after her team lost a big hockey game. Clearly, the moral of the story is that emotions – even negative ones like sadness – are necessary for dealing with life's ups and downs.

Pixar's movie is also a triumph for science education. It's not perfect (there's no biological basis for a 'Core Memory' or the 'Islands of Personality', for instance) but it's still a very clever film. Analogy is a powerful tool that helps people understand complex concepts in an intuitive way, without jargon, and Inside Out has managed to teach a generation of kids – and adults – how memory works.

Watch the video: 18. Γιατί πιστεύουμε στα ζώδια (January 2022).