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Journal of Neuroscience, Vol 14, 7067-7076, Copyright © 1994 by Society for Neuroscience
The metabotropic glutamate receptor types 2/3 inhibit L-type calcium channels via a pertussis toxin-sensitive G-protein in cultured cerebellar granule cells
P Chavis, H Shinozaki, J Bockaert and L Fagni
Centre CNRS-INSERM de Pharmacologie et d'Endocrinologie, Montpellier, France.
Modulation of Ca2+ channels by metabotropic glutamate receptors (mGluRs)
was investigated in cerebellar granule cells using the cell- attached
configuration of the patch-clamp technique. Experiments were performed in
the absence of external Ca2+ and Ba2+ was used as charge carrier. Bath
applied glutamate or (1S,3R) trans-1-aminocyclopentane- 1,3-dicarboxylic
acid (1S,3R t-ACPD) inhibited Ca2+ channels activated by depolarizing
pulses. These channels were sensitive to dihydropyridines and displayed a
23 pS conductance. This effect was mimicked by
(2S,1'S,2'S)-2-(carboxycyclopropyl)glycine (L-CCG-I), a selective agonist
of mGluR2/R3 receptors, but not by quisqualate at a concentration that
stimulated inositol phosphate (InsP) synthesis, showing that mGluR1 and
mGluR5 did not participate to this mechanism. The phosphodiesterase
inhibitor, isobutylmethylxanthine (IBMX), did not alter the action of the
mGluR agonists and biochemical measurements showed that 1S,3R t-ACPD, in
the presence of IBMX, decreased cAMP formation in such a small amount that
this change could not explain the almost complete inhibition of the channel
activity observed under similar experimental conditions. Moreover,
whole-cell recorded L-type Ca2+ currents were inhibited by L-CCG-I, in the
presence of 1 mM intracellular cAMP. These observations were consistent
with the hypothesis that cyclic nucleotide second messengers were not
involved in this effect. Neither the protein kinase C activator
phorbol-12,13- dibutyrate (PDBU) nor the phosphatase inhibitor okadaic acid
affected the action of 1S,3R t-ACPD. The inhibitory action of 1S,3R t-ACPD
was abolished by pertussis toxin (PTX). These results suggest that mGluR2
or mGluR3 receptors suppress the activity of L-type Ca2+ channels by a
mechanism involving Gi or G(o) proteins. A likely direct effect of G-
proteins on the channels is discussed.
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