The tetanus toxin tetanospasmin blocks the release of the neurotransmitter (GABA

Question

The tetanus toxin tetanospasmin blocks the release of the neurotransmitter (GABA) that inhibits motor neurons and decreases muscle contraction. This causes persistence of the signal to contract and the resulting violent muscle contraction known as tetanic spasm. First, explain what happens during normal muscle contraction. Next, compare normal muscle contraction with muscle contraction caused by the action of tetanospasmin on motor neurons. Finally, how is muscle contraction due to tetanospasmin compare to sustained contraction of muscle cells during rigor mortis?

Explanation / Answer

NORMAL MUSCULAR CONTRACTION:

1. Action potential received at the presynaptic motor neuron terminal which opens Voltage-gated calcium channels.

2. Ca2+ ions flow into the cytoplams of presynaptic neurons form extracellular fluid.

3. Influx of Ca2+ causes fusion of vesicles through VSNARE protein to membrane and empties the vesicle's content (acetylecholine) int the synaptic cleft (exocytosis).

4. Synaptobrevin is an integral V-SNARE, which necessary for vesicle fusion of membrane.

5.Sarcolemma membrane of muscles contain AChRs receptors to receive acetylecholine from synaptic cleft causing a cascade that results muscle contraction.

6. GABA is also secondary messenger like acetylcholine that inhibits motor neurons and decrease muscle contraction.

MUSCULAR CONTRACTION DUE TETANOSPASMIN ON MOTOR NERVE:

1. Tetanus toxin is taken up into nerve terminal of motor neuron.

2. This toxin transported across synapses and taken up by nerve endings targets protein synaptobrevin/VSNAR,

3. Tetanus toxin cleaves synaptobrevin and inhibits neurotransmitters in inhibitory muscles.

4. This toxin blocks the release of GABA that lead to inhibition of motor neurons.

5. This causes hyper activity and to increased muscle activity in the form of rigidity and spasms.

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