Explain how resting membrane potential (RMP) is achieved in a cell. Include the

Question

Explain how resting membrane potential (RMP) is achieved in a cell. Include the channels/transporters involved, how they work, the resulting on membrane potential, and why RMP is important to signaling in the neuron. Why is cessation of signaling important? How is resting membrane potential restored after an action potential? What re the fates of neurotransmitters in the synaptic cleft that prevent a signal from continuing? Give a full explanation of what causes an action potential to travel unidirectionally down the axon. Be sure your explanation includes how an action potential moves down the axon.

Explanation / Answer

Answer: 1. RMP is a result of ion concentrating (Na+, K+) inside and outside of a cell. This happens in synapses where the nerve impulses causes Na+ to enter into the cell resulted depolarization then create the impulse.
The charge difference between inside the neuron body and the outside, the differences makes the depolarization and repolarization patterns of RMP. RMP is negative due to the K+ accumulation inside of a cell and the sole increase of Na+ outside. This causes the diffusion of K+ to outside and Na+ to the opposite way, reason is neurons are having many K+ leakage channels than there are Na+ ions.

This interplay between these two ions maintains a negatively-charged membrane inside of a cell; this helps in the homeostasis of RMP.

Approx there is a negative charge of 70 mV on an average, although it changes among the neuron type and species. Main factors to summarize here is i) concentration of ions, ii) the permeability of ions, or ion conductance through specific channels and iii) Electronic pumps (Na+/K+ -ATPase and Ca++ - transport pumps).

2. The signal cessation is because of the resting time needed, from a neuron to fire indefinitely to a stimulant, the mechanism that checks the switch between that. There are three factors associated with it, one is Diffusion, where the neurotransmitters escapes the synapse into nearby extracellular fluid astrocytes to CNS, where it gets absorbed and returns back to neurons. The second factor is reuptake, here mono amine oxidase helps and thirdly there is degradation, enzyme AchE plays the part.

As we have discussed in the first question about the RMP, here we are looking into the mechanism again. As we know the negative membrane potentials about RMP, now when the cells are hyperpolarized, the K+ ion channels take care, so these leaky K+ ion channels are responsible here determining the membrane potential largely. The coordination of k++ and Na+ ion channels closes the doorway permanently, except the time when a action potential is getting generated, this is how it functions.

The Fate of neurotransmitters in the synaptic cleft that prevents the signal from continuing is depends on the nerve-to-nerve impulses and their release and close channels. Here we are talking about the neurotransmitters, the chemical impulses where a presynaptic neuron releases them and the postsynaptic neuron or target cell gets the signal. This chemicals use in the synaptic cleft is depending on the membrane potential after the action potential is restores back to normal there are three different mechanisms that applies to them, these are briefed as follows.

The transmitters may diffuse away from the synaptic cleft, or being taken up by the presynpatic neuron and thirdly they are degraded by the enzymes.

3. So far we know that how a RMP is a negative value and thereby the interplay between the ions at the synaptic cleft. To generate an Action Potential (AP) there is a minimum threshold value, -55mV, this graded potential change can produce an AP. In the second question we have discussed about the three phases of AP, where the depolarization is the first action, followed by there is an event of hyper polarization or refractory period in which new AP’s are not generated.

Now the interesting part is AP’s are mostly generated in the axon hillock. The change in membrane potential triggers reaching the threshold due to graded potential. Then the AP’s become self propagating, this means one potential triggers the neighboring membrane areas turns to be another AP.

4 steps are involved here; the resting stage is the initial one, the threshold voltage reaches, gated Na+ ions channels begin to open, influx of Na+ is next. Furhter the depolarization increase membrane permeability for Na+ to 1000 times. Membrane potential turns from -70 to +50 mV, later the sodium gates begin to close as less sodium comes at the end of it, membrane loses its permeability for ions, finally it stops. Slowly the resting potential shoots up with the help of potassium ions.

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