Question

The tetanus toxin tetanospasmin blocks 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. Compare the sustained contraction of muscle cells in rigor mortis with muscle contraction caused by the action of tetanospasmin on motor neurons.

Answer 1

Tetanospasmin causes muscle contractions by inhibiting inhibitory neurotransmitters like GABA, leading to uncontrollable muscle contractions, while rigor mortis results from a depletion of ATP post-mortem, causing muscles to stiffen.

Step-by-step explanation:

The effect of tetanospasmin, a neurotoxin produced by Clostridium tetani, on muscle contraction can be compared to the sustained contraction observed in rigor mortis. Tetanospasmin blocks the release of inhibitory neurotransmitters like GABA and glycine at the neuromuscular junction, causing muscles to remain contracted uncontrollably. This is because the motor neurons continue to stimulate the muscles without the inhibitory signals that would normally allow them to relax, leading to tetanic spasms.

In contrast, rigor mortis arises after death due to a lack of ATP, which is necessary to detach myosin heads from actin filaments within muscle fibers after contraction. Consequently, the muscles become stiff and locked in place until enzymes start to break down the muscle tissue, which leads to the relaxation of the muscles several hours later. While tetanospasmin-induced contractions result from a biochemical blockage of neuronal inhibitory signals, rigor mortis is a result of ATP depletion.