Electrophysiological recordings of Ca<sup>2+</sup> currents
Parekh AB.
© 2006 by Taylor & Francis Group, LLC. The opening of plasmalemmal Ca2+ channels has profound effects on cell function. First and most importantly, an increase in cytoplasmic Ca2+ concentration is used as a key signaling messenger in virtually every cell through the phylogenetic tree, where it regulates a diverse array of fundamental physiological processes such as neurotransmitter release, muscle contraction, gene transcription, and cell growth and proliferation [1]. Second, when a Ca2+ channel opens, the inward flux of Ca2+ often depolarizes the membrane potential thereby affecting membrane excitability [2]. Finally, Ca2+ channels have fundamental roles in cell signaling that do not require ion permeation. In the T-tubules of skeletal muscle, the intracellular domain between loops II and III of the L-type calcium channel (Cav 1.1) can physically interact, ostensibly via the intermediary protein triadin, with ryanodine type I receptors in the sarcoplasmic reticulum. Depolarization of the T-tubules results in a conformational change in the L-type, that is, channel propagated rapidly to the ryanodine receptor, resulting in Ca2+ release [3].