Each living cell needs access to nerve, artery, and vain. Nerve supplies the imp

Question

Each living cell needs access to nerve, artery, and vain. Nerve supplies the impulse / signal, and the cell responds. How is cellular consciousness maintained within a homeostatic balance restoration? Specifically, what roles does the sodium/potassium pump play, and how does K+ flux influence depolarizing and hyperpolarizing phases within cellular recovery phases after the nerve conduction ceased, regardless of the stimulus amplitude? Each living cell needs access to nerve, artery, and vain. Nerve supplies the impulse / signal, and the cell responds. How is cellular consciousness maintained within a homeostatic balance restoration? Specifically, what roles does the sodium/potassium pump play, and how does K+ flux influence depolarizing and hyperpolarizing phases within cellular recovery phases after the nerve conduction ceased, regardless of the stimulus amplitude?

Explanation / Answer

In the most narrow sense of the word, a reflex, is an involuntary, unpremediated, unlearned, 'built-in" response to a stimulus. The pathway mediating a reflex is known as the reflex arc. An intergrating center often receives signals from many receptors, some of which may be responding to quite different types of stimuli. Thus, the output of an intergrating center reflects the net effect of the total afferent input, that is, it represents an integration of numerous bits of information. The output of an integrating center is sent to the last component of the system, a device whose change in activity constituents the overall response of the system. This component is known as an effector. The information going from an integrating center to an effector is like a command directing the effector to alter its activity. The pathway along which this information travels known as the efferent pathway.

Action potentials result from the a transient change in membrane ion permeability, whereas concentration gradients remains unchanged. In the resting state, the open channels in the plasma membrane are predominantly those that are permeable to potassium and chloride ions. Almost all the sodium ion channels are closed, and the resting potential is therefore much closer to the potassium equilibrium potential than to the sodium equilibrium potential. During an action potential, however, the membrane permeabilities to sodium and potassium ions are markedly altered.

The depolarizing phase of the action potential is due to the opening of sodium channels, increasing the membrane permeability to sodium ions several hundredfold. This allows some sodium ions to rush into the cell. During this period, therefore, more positive charge enters the cell in the form of sodium ions than leaves in the form of potassium ions, and the membrane potential depolarizes. It may even overshoot, becoming positive on the inside and negative on the outside of the membrane. In this phase the membrane potential approaches but does not quite reach the sodium equilibrium potential.

Now, closure of sodium channels restores the membrane potential to its resting level since potassium flux out would then exceed sofium flux in. However, the process is speeded up by the simultaneous increase in potassium permeability. These two events, inactivation of the sodium channels and opening of additional potassium channels, lead to a potassium diffusion out of the cell that is much greater than the sodium diffusion in, rapidly returning the membrane potential to its resting potential. After the sodium channels have closed, at least some of the additional potassium channels are still open, and there is generally a small hyperpolarising overshoot of the membrane potential in nerve cells.

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