Ca^2+ diffusion in a nerve terminal
In a number of fundamental physiological processes such as secretion and muscle contraction, \(Ca^{2+}\) plays a critical regulatory role. During muscular contraction, the intracellular concentration of free \(Ca^{2+}\) increases. Excess \(Ca^{2+}\) is transiently sequestered in several intracellular sites such as the mitochondria and the sarcoplasmic reticulum, a system of membranous sacs of specialized smooth endoplasmic reticulum. An important physiological process which is less well understood than contraction in skeletal muscle is the management of \(Ca^{2+}\) in presynaptic nerve terminals. Recent evidence suggests that nerve terminals also have sites of ATP-dependent, nonmitochondrial \(Ca^{2+}\) sequestration. The leading candidate for such a site is the intraterminal smooth endoplasmic reticulum (SER) which is organized into a vesicular structure akin to that of the sarcoplasmic reticulum of skeletal muscles. It is thought that the SER has a high affinity but limited capacity for the storage of \(Ca^{2+}\), while the mitochondria have a low affinity but a large capacity. Thus in the short term it is anticipated that the SER's role in the sequestration of \(Ca^{2+}\) is of considerable importance.
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