Lionel studies the effect of the snake venom alpha-bungarotoxin on the neuromuscular junction. When he adds venom to a nerve muscle preparation, the neurotransmitter acetylcholine (ACh) is released from the axon terminal, but stays in the synaptic gap. The muscle does not contract. What is the best explanation for these observations? Alpha-bungarotoxin stimulates the activity of the enzyme acetylcholinesterase breaking down ACh before it can bind to the receptor. Alpha-bungarotoxin inhibits the fusion of the vesicles to the presynaptic membrane. Alpha-bungarotoxin stimulates the re-uptake of ACh removing it quickly from the synapse. Alpha-bungarotoxin binds to the receptor blocking access of ACh.
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The venom of many cobras contains a potent neurotoxin that binds to ligand-gated Na+ channels, causing them to open. Unlike ACh, which binds to and then rapidly unbinds from ligand-gated Na+ channels, the neurotoxin tends to remain bound to ligand-gated Na+ channels. How does this neurotoxin affect the nervous system's ability to stimulate skeletal muscle contraction? How does it affect the ability of skeletal muscle fibers to respond to stimulation?
Adi S.
Several snake venoms contain toxins which blocks acetylcholine receptors at the neuromuscular junction. The presence of these toxins would directly interfere with the ability to: a initiate skeletal muscle contraction b relax cardiac muscle after contraction c control smooth muscle contraction d release acetylcholine from motor neurons e generate action potentials in motor neurons
Cobra venom helps the snake secure food by binding to acetylcholine receptors on the diaphragm of a bite victim, leading to the loss of function of the diaphragm muscle tissue and eventually death. In order to develop more potent antivenins, scientists have studied what happens to the toxin once it has bound the acetylcholine receptors. They have found that the toxin is released from the receptor in a process that can be described by the rate law $$Rate $=k[\text { acetylcholine receptor-toxin complex }]$$ If the activation energy of this reaction at $37.0^{\circ} \mathrm{C}$ is $26.2 \mathrm{kJ} /$ mol and $A=0.850 \mathrm{s}^{-1},$ what is the rate of reaction if you have a 0.200-M solution of receptor-toxin complex at $37.0^{\circ} \mathrm{C} ?$
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