voltage-gated ion channels
NA plus channels open in response to a change in the membrane potential, causing the channel to undergo conformational changes that lead to its opening. This change in membrane potential can be initiated by various stimuli, such as neurotransmitter binding or depolarization of the cell.
The membrane potential is determined by the distribution of ions across the membrane and their relative permeabilities. In both cases, if there are only potassium (K⁺) channels and no sodium (Na⁺) channels, the membrane potential will primarily reflect the equilibrium potential for potassium, which is governed by the Nernst equation. Thus, whether there are 3 K⁺ channels or 5 K⁺ channels, the increased conductance from more K⁺ channels does not change the equilibrium potential for potassium, leading to the same membrane potential in both scenarios.
Sodium channels. A neuron's membrane potential may depolarize for many reasons (neurotransmitters, mechanical deflection, electrical synapse, etc). When that membrane depolarizes to the point of its threshold of activation, then voltage gated channels open up an allow an influx of sodium into the cell. This rapidly depolarizes the cell's membrane, causing that upward peak or rising phase to occur.
Opening or closing of ion channels at one point in the membrane produces a local change in the membrane potential, which causes electric current to flow rapidly to other points in the membrane.
Depolarization is the initial phase of the action potential characterized by a rapid influx of sodium ions into the cell, causing a change in membrane potential from negative to positive. This occurs when voltage-gated sodium channels open in response to a threshold stimulus, leading to the depolarization of the cell membrane.
Local responce is a small change in membrane potential caused by a subthreshold stimulus.
A sudden increase in membrane potential, typically from a resting membrane potential of around -70mV to a threshold potential of around -55mV, triggers the opening of voltage-gated sodium channels leading to depolarization and initiation of an action potential.
During an action potential, the neuron undergoes a rapid change in membrane potential as sodium ions rush into the cell, leading to depolarization. Subsequently, potassium ions move out of the cell, repolarizing the membrane back to its resting state. This rapid change in membrane potential allows for the transmission of electrical signals along the neuron.
The stimuli that can change the resting membrane potential of a cell include changes in ion concentrations inside or outside the cell, neurotransmitter binding to receptors, and mechanical deformation of the cell membrane. These changes can lead to the opening or closing of ion channels, altering the flow of ions across the membrane and affecting the cell's resting membrane potential.
depolarization
The action potential has 5 main phases:1) stimulation/rising phase - depolarization caused by influx of sodium ions at the axon hillock; potential increases from a resting potential of -70 mV2) peak phase - depolarization and membrane potential reaches a peak, with sodium channels open maximally, at about +40 mV3) falling phase - potassium channels open in response, causing a subsequent reduction in membrane potential, and the neuron begins to repolarize4) hyperpolarization/undershoot phase - more potassium channels stay open after sodium channels close, causing a hyperpolarization of the neuronal membrane, bringing the potential down below its initial resting potential (below -70 mV)5) refractory phase - potassium channels begin to close, allowing the membrane potential to revert back to the resting potential of -70 mV; during this phase, the probability of the nerve being able to refire is extremely low, thus allowing for a delay between action potentials
The action potential is generated when a stimulus causes a change in the electrical potential across the cell membrane, resulting in the opening of voltage-gated ion channels. This allows an influx of sodium ions, causing depolarization of the membrane and initiation of the action potential.