Suppose you were a neuroscientist and were given a sample of a new sna...
When the neurotoxin reaches the Neuromuscular junction then it induces the release of more amount of Ca ions in the pre syanaptic membrane due to which more amount of neurotransmitter is released (from vesicles) at synapse which increases the magnitude of depolarisation at synapse or it can also act as a duplicate of neurotransmitter and can cause increase of depolarisation which depends upon the similarity in their molecular function and structure
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Suppose you were a neuroscientist and were given a sample of a new sna...
Option b
actually the when neurotoxin reaches the Neuromuscular junction then it induces the release of more amount of Ca ions in the pre syanaptic membrane due to which more amount of neurotransmitter is released (from vesicles) at synapse which increases the magnitude of depolarisation at synapse
or it can also act as a duplicate
of neurotransmitter and can cause increase of depolarisation ..depends upon the similarity in their molecular function and structure
Suppose you were a neuroscientist and were given a sample of a new sna...
Explanation:
The most likely explanation for the snake venom increasing the magnitude of the normal depolarizing excitatory response at a synapse is that it is binding with the neurotransmitter receptors to mimic the action of the neurotransmitter.
Neurotransmitter receptors:
Neurotransmitter receptors are proteins located on the postsynaptic membrane of a synapse. They are responsible for receiving the neurotransmitter released by the presynaptic neuron and initiating a response in the postsynaptic neuron. There are two types of neurotransmitter receptors: ionotropic receptors and metabotropic receptors.
Ionotropic receptors:
Ionotropic receptors are ligand-gated ion channels that open in response to the binding of a neurotransmitter. When a neurotransmitter binds to an ionotropic receptor, it causes the ion channel to open, allowing ions to flow into or out of the neuron. This change in ion flow leads to a change in the membrane potential of the postsynaptic neuron, either depolarizing or hyperpolarizing it.
Snake venom effect:
In this scenario, the snake venom is increasing the magnitude of the normal depolarizing excitatory response. This suggests that the venom is binding with the neurotransmitter receptors and mimicking the action of the neurotransmitter. By binding to the receptors, the venom is likely causing the ion channels to open for a longer duration or allowing more ions to flow through the channels, resulting in a larger depolarizing response.
Other possibilities:
The other options provided (blocking release of the neurotransmitter, acting to break down the neurotransmitter, preventing the presynaptic action potential from arriving at the synapse) are less likely explanations for the observed effect. If the venom were blocking the release of the neurotransmitter, there would be a decrease in the magnitude of the depolarizing response. If it were breaking down the neurotransmitter or preventing the presynaptic action potential from arriving at the synapse, there would likely be no response or a decrease in the magnitude of the response.
Conclusion:
In summary, the most likely explanation for the snake venom increasing the magnitude of the normal depolarizing excitatory response is that it is binding with the neurotransmitter receptors to mimic the action of the neurotransmitter. This leads to a larger depolarizing response in the postsynaptic neuron.
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