Medical Physiology - Nerve Action Potential

Medical Physiology - Nerve Action Potential
Nerve signals are conveyed through action potentials, which are fast alterations in membrane potential. Each action potential commences with an abrupt transition from the typical resting negative potential to a positive membrane potential, followed by a nearly instantaneous return to the resting negative potential. The sequential phases of the action potential are as follows:
• Resting phase. This represents the resting membrane potential prior to the initiation of the action potential.
• Depolarization phase. At this moment, the membrane abruptly becomes permeable to sodium ions, permitting a substantial influx of positively charged sodium ions into the axon, resulting in a quick increase in potential in the positive direction.
• Repolarization phase. Within a few ten-thousandths of a second after the membrane attains high permeability to sodium ions, the sodium channels commence closure while the potassium channels open to a greater extent than usual. The swift efflux of potassium ions to the exterior reinstates the typical negative resting membrane potential.
Voltage-gated sodium and potassium channels undergo activation and inactivation throughout the progression of an action potential. The essential element for both depolarization and repolarization of the neuronal membrane during the action potential is the voltage-gated sodium channel. The voltage-gated potassium channel significantly contributes to the acceleration of membrane repolarization. These two voltage-gated channels exist alongside the Na⁺-K⁺ pump and the Na⁺-K⁺ leak channels that determine the membrane's resting permeability.
The events that precipitate the action potential can be summarized as follows.
• In the resting state, prior to the initiation of the action potential, the conductance for potassium ions is approximately 100 times greater than that for sodium ions. This results from significantly increased leaking of potassium ions compared to sodium ions through the leak channels.
• At the initiation of the action potential, the sodium channels rapidly activate, permitting an increase in sodium permeability of up to 5000-fold (also referred to as sodium conductance). The inactivation process subsequently occludes the sodium channels within only fractions of a millisecond. The initiation of the action potential triggers the voltage gating of potassium channels, leading to their gradual opening. Upon conclusion of the action potential, the restoration of the membrane potential to a negative state prompts the potassium channels to revert to their previous configuration, albeit after a delay.

A positive-feedback loop initiates the opening of sodium channels.
Should any event induce the membrane potential to ascend from 90 millivolts towards the zero level, the increasing voltage itself prompts the opening of many voltage-gated sodium channels. This facilitates the fast influx of sodium ions, resulting in an additional increase in membrane potential, so activating more voltage-gated sodium channels. This mechanism constitutes a positive-feedback loop that persists until all voltage-gated sodium channels are engaged. An action potential is initiated only upon reaching the threshold potential. This occurs when the quantity of sodium ions infiltrating the nerve fiber The quantity of potassium ions exiting the fiber exceeds the influx of potassium ions. An abrupt elevation in the membrane potential of a major nerve fiber from –90 millivolts to around –65 millivolts typically triggers a rapid onset of the action potential. A membrane potential of –65 millivolts is identified as the stimulation threshold. An action potential cannot be generated while the membrane remains depolarized from the preceding action potential. Immediately following the initiation of the action potential, the sodium channels undergo inactivation, rendering any excitatory signal supplied to these channels ineffective in opening the inactivation gates. The sole situation that can reactivate them is when the membrane potential reverts to or nearly to the initial resting membrane potential level.
Subsequently, during another brief fraction of a second, the inactivation gates of the channels open, allowing for the initiation of a fresh action potential.
• Absolute refractory phase. An action potential cannot be generated during the absolute refractory period, regardless of the stimulus strength. The refractory period for big myelinated nerve fibers is around 1/2500 of a second, allowing for a maximum transmission of about 2500 impulses per second
. • Relative refractory phase. This interval succeeds the absolute refractory period. During this period, stimuli of greater intensity than usual can activate the nerve fiber, leading to the initiation of an action potential.