Potassium resting membrane/action potentials

Keywords Action potential Calcium Glia Ion channel LTP Neuron Neurotransmitter Potassium Resting membrane potential Sodium Structure Synapse... 

K Channels belong to a class of membrane proteins that form highly K-selective pores in membranes. All known K Channels are composed of several (usually four) pore forming alpha subunits and auxiliary beta subunits. K Channels play an essential role in cellular excitability, being involved in repolarization of Action Potentials and setting the cell resting potential as well as contributing to potassium homeostasis. 

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... 

Thus, a 10 1 transmembrane gradient of a single monovalent ion, say potassium, will generate a membrane potential of 58 mV. See Resting Potential Action Potential Depolarization Threshold Potential Nernst Equation Goldman Equation Patch-Clamp Technique... 

In normal atrial and ventricular myocytes, phase 4 is electrically stable, with the resting membrane potential held at approximately -90 mV and maintained by the outward potassium leak current and ion exchangers previously described. It is during phase 4 that the Na+ channels necessary for atrial and ventricular myocyte depolarization recover completely from inactivation. In myocytes capable of automaticity, the membrane potential slowly depolarizes during this period to initiate an action potential (discussed later). 

Adenosine receptors are found on myocytes in the atria and sinoatrial and A-V nodes. Stimulation of these receptors acts via a G-protein signaling cascade to open an acetylcholine-sensitive outward potassium current. This leads to hyperpolarization of the resting membrane potential, a decrease in the slope of phase 4 spontaneous depolarization, and shortening of the action potential duration. 

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