What are synaptic toxins?
Synaptic toxins / neurotoxins are substances that interfere with the course of natural excitation transmission in synapses.
In the animal kingdom countless animals and plants make use of such neurotoxins: For defense (bees and wasps), for killing prey animals (poisonous snakes, poison dart frogs, jellyfish, poison spiders) and for protection against potential insect enemies and pests (belladonna, yew, green tuber-leaf fungus) ,
Nerve drugs differ mainly in their mode of action at the synapse. Functional influence with negative consequences is possible almost everywhere in the synapse: at the synaptic endpoint, in the synaptic cleft and at the postsynapse.
Different modes of action of neurotoxins
Lack of delivery of neurotransmitters
Botulinum toxin: prevents the release of the neurotransmitter acetylcholine into the synaptic cleft. The venom on the presynaptic membrane blocks the exocytosis of the synaptic vesicles with the membrane. As a result, depending on the severity of the poisoning less or no more neurotransmitters are released. As a result, no action potentials are forwarded any more and it comes to the paralysis of the muscles.
Botulinum toxin (lat. Botulus = sausage) owes its name to the bacterium Clostridium botulinum, which proliferates in old sausage preserves and thereby produces the botulinum. Thrown canned foods are therefore no longer suitable for consumption and to dispose of!
In addition, low-dose Botox is used as a neurotoxin for cosmetic procedures.
Opening of the calcium channels
Alpha latrotoxin: provides in the presynaptic end-point for permanent opening of calcium channels. Thus, a continuous incoming excitation is simulated, which leads to a continuous delivery of neurotransmitters into the synaptic cleft. As a result, it comes to muscle cramps.
Latroxin is used by several spider species to kill prey, such as the Black Widow.
Inhibition of enzymes that cleave neurotransmitters
Insecticide parathion (E 605): inhibits in the synaptic cleft the activity of the enzyme acetylcholinesterase, which is responsible for the cleavage of acetylcholine in choline and acetic acid. As long as the transmitter acetylcholine is located in the synaptic cleft and thus able to bind to the receptors, sodium ions enter the post-synaptic membrane through the opened sodium channels. This causes a permanent depolarization of the following dendrites. It comes to muscle cramps.
Competing neurotransmitters at the receptor
Atropine: competes with other transmitters in the synaptic cleft and blocks the receptors of the postsynaptic membrane. It is chemically similar to the neurotransmitter acetylcholine and can therefore dock to the same receptors. In contrast to acetylcholine, however, it has no effect on the opening of the sodium channels of the postsynaptic membrane, whereby the depolarization is absent. The poison Atropin is in the fruits of the Black Belladonna.