Jump to content

Afterhyperpolarization

From Wikipedia, the free encyclopedia
This is an old revision of this page, as edited by Diptanshu Das (talk | contribs) at 15:52, 18 May 2013 ({{unreferenced|date=May 2013}}). The present address (URL) is a permanent link to this revision, which may differ significantly from the current revision.
Schematic of an electrophysiological recording of an action potential, showing the various phases that occur as the voltage wave passes a point on a cell membrane. The afterhyperpolarisation is one of the processes that contribute to the refactory period.

Afterhyperpolarization, or AHP, describes the hyperpolarization phase of a neuron's action potential where the cell's membrane potential falls below the normal resting potential. This is also commonly referred to as an action potential's undershoot phase. Afterhyperpolarization in part causes the neuronal refractory period, the time period following an action potential during which a neuron cannot initiate a subsequent action potential.

During the action potential, the raised voltage opens many more voltage-gated K+ channels than usual, many of which do not close immediately when the membrane returns to its normal resting voltage. In addition, other potassium channels open in response to the influx of Ca2+ during the action potential. The K+ permeability of the membrane is transiently unusually high, driving the membrane voltage Vm even closer to the K+ equilibrium voltage EK. Hence, hyperpolarization persists until the membrane K+ permeability returns to its usual value.[1]

Both medium and slow AHP currents can be demonstrated in neurons.[2] The SK channel, a Ca2+-activated potassium channel, is the major mediator of AHP currents, although other candidate mediators have been suggested.

See also

References

  1. ^ Purves et al., p. 37; Bullock, Orkand, and Grinnell, p. 152.
  2. ^ M. Shah, and D. G. Haylett. Ca2+ Channels Involved in the Generation of the Slow Afterhyperpolarization in Cultured Rat Hippocampal Pyramidal Neurons. J Neurophysiol 83: 2554-2561, 2000.