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J Neurophysiol 81: 2903-2913, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 81 No. 6 June 1999, pp. 2903-2913
Copyright ©1999 by the American Physiological Society

Group I mGluR Activation Causes Voltage-Dependent and -Independent Ca2+ Rises in Hippocampal Pyramidal Cells

Riccardo Bianchi, Steven R. Young, and Robert K. S. Wong

Department of Physiology and Pharmacology, State University of New York Health Science Center at Brooklyn, Brooklyn, New York 11203

Bianchi, Riccardo, Steven R. Young, and Robert K. S. Wong. Group I mGluR Activation Causes Voltage-Dependent and -Independent Ca2+ Rises in Hippocampal Pyramidal Cells. J. Neurophysiol. 81: 2903-2913, 1999.Group I mGluR activation causes voltage-dependent and -independent Ca2+ rises in hippocampal pyramidal cells. Application of the metabotropic glutamate receptor (mGluR) agonist (1S,3R)-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD) or the selective group I mGluR agonist (S)-3,5-dihydroxyphenylglycine (DHPG) depolarized both CA3 and CA1 pyramidal cells in guinea pig hippocampal slices. Simultaneous recordings of voltage and intracellular Ca2+ levels revealed that the depolarization was accompanied by a biphasic elevation of intracellular Ca2+ concentration ([Ca2+]i): a transient calcium rise followed by a delayed, sustained elevation. The transient [Ca2+]i rise was independent of the membrane potential and was blocked when caffeine was added to the perfusing solution. The sustained [Ca2+]i rise appeared when membrane depolarization reached threshold for voltage-gated Ca2+ influx and was suppressed by membrane hyperpolarization. The depolarization was associated with an increased input resistance and persisted when either the transient or sustained [Ca2+]i responses was blocked. mGluR-mediated voltage and [Ca2+]i responses were blocked by (+)-alpha -methyl-4-carboxyphenylglycine (MCPG) or (S)-4-carboxy-3-hydroxyphenylglycine (4C3HPG). These data suggest that in both CA3 and CA1 hippocampal cells, activation of group I mGluRs produced a biphasic accumulation of [Ca2+]i via two paths: a transient release from intracellular stores, and subsequently, by influx through voltage-gated Ca2+ channels. The concurrent mGluR-induced membrane depolarization was not caused by the [Ca2+]i rise.




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