Botulism and tetanus toxins both affect the neuromuscular junctions. Perform an Internet search to determine how each of these toxins affects the neuromuscular junctions
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The neuromuscular junction is a contact between a nerve and a muscle.
Neurotransmitters are made in the terminal end of the nerve and are stored in tiny vesicles so that they can be released whenever an action potential comes along. When the neurotransmitter is released, it moves across the short synaptic gap and binds to a receptor protein on the postsynaptic membrane. There are dozens of neurotransmitters in the nervous system; some are excitatory and some are inhibitory.
Botulism and tetanus toxins block neurotransmitter release. Both botulism and tetanus toxins are produced by endospore-forming bacteria belonging to the
Clostridium genus. Clostridium botulinum produces a toxin most commonly associated with home-canned food products. Botulism toxin affects the neuromuscular junction by inhibiting acetylcholine from being released in the neuromuscular junction. This inhibits muscle contraction because the neurotransmitter acetylcholine is needed
to cause muscle contraction. Animals with botulism have flaccid paralysis or weak muscles.
Clostridium tetani produces a toxin that restrains the release of inhibitory
neurotransmitters glycine and GABA. This causes the muscles to remain contracted and appear spastic. Tetanus is sometimes referred to as lockjaw because early victims of this disease presented with loss of ability to open their jaws.
Other things that affect the neuromuscular junction are black widow spider toxin, nerve gas, organophosphate insecticides (see Chapter 15), and atropine (see Chapter 7).
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