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Endogenous Intracellular Calcium Buffering and the Activation/Inactivation of HVA Calcium Currents in Rat Dentate Cyrus Granule Cells

A B ST R ACT Granule cells acutely dissociated from the dentate gyrus of adult rat brains displayed a single class of high-threshold, voltage-activated (HVA) Ca 2+ channels. The kinetics of whole-cell Ca ~+ currents recorded with pipette solutions containing an intracellular ATP regenerat ing system but devoid of exogenous Ca ~+ buffers, were fit best by Hodgkin-Huxley kinetics (m2h), and were indistinguishable from those recorded with the nystatin perforated patch method. In the absence of exogenous Ca ~+ buffers, inactivation of HVA Ca ~+ channels was a predominantly Ca~+-dependent process. The contribution of endogenous Ca ~+ buffers to the kinetics of inactivation was investigated by comparing currents recorded from control cells to currents recorded from neurons that have lost a specific Ca ~+binding protein, Calbindin-D~8 ~ (CaBP), after kindling-induced epilepsy. Kindled neurons devoid of CaBP showed faster rates of both activation and inactivation. Adding an exogenous Ca 2+ chelator, 1,2-bis-(2-aminophenoxy)ethane-N,N,N',N'tetraacetic acid (BAPTA), to the intracellular solution largely eliminated inactivation in both control and kindled neurons. The results are consistent with the hypothesis that endogenous intraneuronal CaBP contributes significantly to submembrane Ca 2+ sequestration at a concentration range and time domain that regulate Ca ~+ channel inactivation.