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The rapid depolarization of the cell, during phase 0, causes the membrane potential to approach sodium's equilibrium potential (i.e. the membrane potential at which sodium is no longer drawn into or out of the cell). As the membrane potential becomes more positive, the sodium channels then close and lock, this is known as the "inactivated" state.
MEF2, Myocyte Enhancer Factor 2, is a transcription factor with four specific numbers such as MEF2A, B, C, and D. Each MEF2 gene is located on a specific chromosome. MEF2 is known to be involved in the development and the looping of the heart (Chen) MEF2 is necessary for myocyte differentiation and gene activation (Black).
Specialised membrane proteins (voltage-gated sodium channels) in the cell membrane selectively allow sodium ions to enter the cell. This causes the membrane potential to rise at a rate of about 300 V/s. As the membrane voltage rises (to about 40 mV) sodium channels close due to a process called inactivation. Phase 1: Rapid repolarisation.
These two relative ion concentration changes slowly depolarize (make more positive) the inside membrane potential (voltage) of the cell, giving these cells their pacemaker potential. When the membrane potential gets depolarized to about -40mV it has reached threshold (cells enter phase 0), allowing an action potential to be generated.
The Purkinje fibers, named for Jan Evangelista Purkyně, (English: / p ɜːr ˈ k ɪ n dʒ i / pur-KIN-jee; [1] Czech: [ˈpurkɪɲɛ] ⓘ; Purkinje tissue or subendocardial branches) are located in the inner ventricular walls of the heart, [2] just beneath the endocardium in a space called the subendocardium.
The G-protein also activates a potassium channel GIRK-1 and GIRK-4, which allows K + to flow out of the cell, making the membrane potential more negative and slowing the pacemaker potential, therefore decreasing the rate of action potential production and therefore decreasing heart rate. [20] A decrease in heart rate is known as negative ...
HCN4 is the main isoform expressed in the sinoatrial node, but low levels of HCN1 and HCN2 have also been reported.The current through HCN channels, called the pacemaker current (I f), plays a key role in the generation and modulation of cardiac rhythmicity, [13] as they are responsible for the spontaneous depolarization in pacemaker action potentials in the heart.
The threshold potential is the potential an excitable cell membrane, such as a myocyte, must reach in order to induce an action potential. [7] This depolarization is caused by very small net inward currents of calcium ions across the cell membrane, which gives rise to the action potential.