3. Throughout the nervous system the predominant mode of neuron to neuron and ne

Question

3. Throughout the nervous system the predominant mode of neuron to neuron and neuron to effector (muscle or gland) transmission involves the conversion of an electrical event in the presynaptic neuron to a chemical event and then back to an electrical event in the postsynaptic cell. Interference with any step in this sequence has significant effects on the nerve and/or effector function. You discover that a toxin causes paralysis. It binds to presynaptic sites and prevents the release of the neurotransmitter from vesicles. Predict the consequences (increase, decrease, no change) of blocking the release of the neurotransmitter at the synapse on the following. Provide a short explanation Parameter Prediction Explain your answer Presynaptic action potential amplitude 1. 2. Presynaptic Ca2 influx 3. Postsynaptic resting potential 4. Post synaptic graded potential 5. Postsynaptic action potential frequency

Explanation / Answer

The following are the steps involved in neurohumoral transmission:

1. Generation and propagation of action potential in the presynaptic neuron

2. Once action potential reaches nerve terminal, it results in the opening of Ca++ channels, causing Ca++ entry which fuses to the vesicles containing neurotransmitters and help them to release the neurotransmitters into synaptic space by a process known as exocytosis.

3. These neurotransmitters bind to specific receptors on the post synaptic membrane resulting in the generation of excitatory post synaptic potential ( Post synaptic graded potential) which helps in the propagation of nerve impulses or stimulation of effector organs ( contraction of muscles or secretion from glands etc).

Now lets look at the questions step by step:

The answers here are predicted considering that the muscle ( post synaptic organ - it is muscle because the question states about paralysis) here is in resting stage.

1. Pre-synaptic action potential amplitude - no change.

As the toxin is blocking the release of neurotransmitter, which usually occurs as a consequence of action potential, the presynaptic action potential amplitude is not affected as it doesnot interfere with generation of action potential.

2. Pre synaptic Ca++ influx: decreases

As the release of neurotransmitters require Ca++ influx in to the presynaptic neuron, this toxin may block Ca++ entry into the presynaptic neuron hus inhibiting exocytosis.

3. Post synaptic resting potential: no change

As the neurotransmitters are not released from the presynaptic neuron, the resting membrane potential of the post synaptic neuron remains unchanged as there is neither depolarization nor repolarization.

4.post synaptic graded potential: no change

Same as above.

5. Post synaptic action potential frequency: no change

As there is no neurotransmitter released, no depolarization of ppstsynatic membrane occurs and hence no action potential is generated.

If the muscle was considered to be in active state before the toxin is given, then the answers for 4th and 5th questions will be " decreases". This is because the previously the muscle was actively contracting which means there were post synaptic graded potential ( excitatory post synaptic potential) which led to generation of action potential which in turn led to contraction. Hence after toxin administration, there wont be any post synaptic potential generated as the neurotransmitter is not released from presynaptic neuron and hence decreased action potential frequency.

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