Abstract
The level of intracellular calcium is the hub of many control processes, providing a transduction of electrical activity into biochemical control. Depolarizing activity in excitable cells activates voltage-dependent calcium currents (Hagiwara and Byerly, 1981; Tsien 1983: McCleskey et al., 1986), which can be regenerative, resulting in a rapid increase in the activity of intracellular calcium ions in the vicinity of the channel. The elevation in intracellular calcium is closely controlled by buffering processes and subsequent extrusion of the calcium (Baker, 1976, 1987) maintaining a low resting level of calcium; uncontrolled and generalized increases in calcium being toxic (Hajos et al., 1986). Under physiological conditions spatially and temporally restricted elevations in the level of free calcium (Chad and Eckert, 1984; Simon and Llinas, 1985) are responsible for control of ion channels and the transduction of electrical activity into responses such as exocytosis and contraction. The increased level of calcium modulates calcium-dependent enzymes, such as those linked to calmodulin (Klee et al., 1980; Stoclet et al., 1986), to alter their activity and hence generate a diversity of responses. The intracellular calcium ions can act as second messengers to control and modulate ionic channels, producing activation (Meech 1978; Colquhoun et al., 1981; Yellen, 1982) or inactivation (Chad and Eckert, 1984), and play a pivotal role in rhythmic activity (Hermann et al., this volume).
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Chad, J. (1988). Control of the Generation and Removal of Calcium-Mediated Inactivation of the Calcium Current in Helix Aspersa Neurons. In: Grinnell, A.D., Armstrong, D., Jackson, M.B. (eds) Calcium and Ion Channel Modulation. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-0975-8_16
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