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J Neurophysiol 79: 695-703, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 79 No. 2 February 1998, pp. 695-703
Copyright ©1998 The American Physiological Society

Characterization of an Intracellular Alkaline Shift in Rat Astrocytes Triggered by Metabotropic Glutamate Receptors

Brian J. Amos and Mitchell Chesler

Department of Neurosurgery and Department of Physiology and Neuroscience, New York University Medical Center, New York, New York 10016

Amos, Brian J. and Mitchell Chesler. Characterization of an intracellular alkaline shift in rat astrocytes triggered by metabotropic glutamate receptors. J. Neurophysiol. 79: 695-703, 1998. The modulation of intracellular pH by activation of metabotropic glutamate receptors was investigated in cultured and acutely dissociated rat astrocytes. One minute superfusion of 100 µM (1S,3R)-1-aminocyclopentane-1,3-dicarboxcylic acid (ACPD) evoked an alkaline shift of 0.13 ± 0.013 (mean ± SE) and 0.16 ± 0.03 pH units in cultured (cortical or cerebellar) and acutely dissociated cortical astrocytes, respectively. Alkalinizations were elicited by concentrations of ACPD as low as 1 µM. The ACPD response was mimicked by S-3-hydroxyphenylglycine (3-HPG) and by (s)-4-carboxy-3-hydroxyphenylglycine (4C-3HPG) but was not blocked by alpha -methyl-4-carboxyphenylglycine (MCPG) or (RS)-1-aminoindan-1,5-dicarboxcylic acid (AIDA), features consistent with an mGluR5 receptor-mediated mechanism. The ACPD-evoked alkaline shift was insensitive to amiloride, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS), and the v-type ATPase inhibitors 7-chloro-4-nitrobenz-2-oxa-1,3-diazol (NBD-Cl), bafilomycin, and concanamycin. The alkaline response persisted in Na+- or Cl--free saline, but was reversibly blocked in bicarbonate-free, N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid (HEPES)-buffered solutions. A bicarbonate-dependent and Na+-independent alkaline shift could also be elicited by either 3 mM caffeine or 1 µM ionomycin. These data suggest that a rise in cytosolic Ca2+ activity is instrumental in triggering the alkalinizing mechanism and that this response is independent of the classic depolarization-induced alkalinization mediated by electrogenic sodium-bicarbonate cotransport.




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