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Ca 2+ ‐Dependent Inactivation of P‐Type Calcium Channels in Nerve Terminals
Author(s) -
Tareilus Erwin,
Schoch Juergen,
Breer Heinz
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.62062283.x
Subject(s) - extracellular , biophysics , calcium , depolarization , intracellular , chemistry , voltage dependent calcium channel , electrophysiology , synaptosome , biochemistry , neuroscience , biology , organic chemistry
Rapid Ca 2+ signals evoked by K + depolarization of rat cerebral cortical synaptosomes were measured by dual‐channel Ca 2+ spectrofluorometry coupled to a stopped‐flow device. Kinetic analysis of the signal rise phase at various extracellular Ca 2+ concentrations revealed that the responsible voltage‐dependent Ca 2+ channels, previously identified as P‐type Ca 2+ channels, inactivate owing to the rise in intracellular Ca 2+ levels. At millimolar extracellular Ca 2+ concentrations the channels were inactivated very rapidly and the rate was dependent on the high influx rate of Ca 2+ , thus limiting the Ca 2+ signal amplitudes to 500–600 n M. A slower, probably voltage‐dependent regulation appears to be effective at lower Ca 2+ influx rates, leading to submaximal Ca 2+ signal amplitudes. The functional feedback regulation of calcium channels via a sensor for intracellular Ca 2+ levels appears to be responsible for the different inhibition characteristics of Cd 2+ versus ω‐agatoxin IVa.