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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.
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.
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 open sodium channels allow more sodium ions to flow into the cell and resulting in further depolarisation, which will subsequently open even more sodium channels. At a certain moment this process becomes regenerative (vicious cycle) and results in the rapid ascending phase of action potential. In parallel with the depolarisation and sodium ...
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.
However this G-protein works by inhibiting, the cAMP pathway, therefore, preventing the sympathetic nervous system from increasing heart rate. As well as this, in the SAN, the G-protein activates specific potassium channel, that opposes action potential initiation (see SAN for more details), thus slowing heart rate. [2]
The cycle is broken when the membrane potential reaches to the sodium equilibrium potential and potassium channels open to re-polarize the membrane potential. This positive feedback loop means that the closer these voltage-gated Na + channels are to each other, the lower the threshold of activation. [1]