Search results
Results from the WOW.Com Content Network
As an action potential (nerve impulse) travels down an axon there is a change in electric polarity across the membrane of the axon. In response to a signal from another neuron, sodium- (Na +) and potassium- (K +)–gated ion channels open and close as the membrane reaches its threshold potential.
In excitable cells, such as neurons, the delayed counterflow of potassium ions shapes the action potential. By contributing to the regulation of the cardiac action potential duration in cardiac muscle, malfunction of potassium channels may cause life-threatening arrhythmias. Potassium channels may also be involved in maintaining vascular tone.
The slope of phase 0 on the action potential waveform (see figure 2) represents the maximum rate of voltage change of the cardiac action potential and is known as dV/dt max. In pacemaker cells (e.g. sinoatrial node cells), however, the increase in membrane voltage is mainly due to activation of L-type calcium channels.
This combination of closed sodium channels and open potassium channels leads to the neuron re-polarizing and becoming negative again. The neuron continues to re-polarize until the cell reaches ~ –75 mV, [2] which is the equilibrium potential of potassium ions. This is the point at which the neuron is hyperpolarized, between –70 mV and –75 mV.
Voltage-gated potassium channels (VGKCs) are transmembrane channels specific for potassium and sensitive to voltage changes in the cell's membrane potential. During action potentials , they play a crucial role in returning the depolarized cell to a resting state.
The potassium channels exhibit a delayed reaction to the membrane repolarisation, and, even after the resting potential is achieved, some potassium continues to flow out, resulting in an intracellular fluid that is more negative than the resting potential, and during which no action potential can begin (undershoot phase/refractory period). This ...
The channels then close, de-inactivate, and regain their ability to open in response to stimulus. The relative refractory period immediately follows the absolute. As voltage-gated potassium channels open to terminate the action potential by repolarizing the membrane, the potassium conductance of the membrane increases dramatically.
At this point, the calcium ion channels close and potassium channels open, allowing outflux of K + and resulting in repolarization. When the membrane potential reaches approximately −60 mV, the K + channels close and Na + channels open, and the prepotential phase begins again. This process gives the autorhythmicity to cardiac muscle.