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The Journal of Neurophysiology Vol. 88 No. 1 July 2002, pp. 107-116
Copyright ©2002 by the American Physiological Society
Department of Psychology and the Neuroscience Research Centre, University of Otago, Dunedin, New Zealand
Ireland, David R. and
Wickliffe C. Abraham.
Group I mGluRs Increase Excitability of Hippocampal CA1 Pyramidal
Neurons by a PLC-Independent Mechanism. J. Neurophysiol. 88: 107-116, 2002. Previous studies have
implicated phospholipase C (PLC)-linked Group I metabotropic glutamate
receptors (mGluRs) in regulating the excitability of hippocampal CA1
pyramidal neurons. We used intracellular recordings from rat
hippocampal slices and specific antagonists to examine in more detail
the mGluR receptor subtypes and signal transduction mechanisms
underlying this effect. Application of the Group I mGluR agonist
(RS)-3,5-dihydroxyphenylglycine (DHPG) suppressed slow- and
medium-duration afterhyperpolarizations (s- and mAHP) and caused a
consequent increase in cell excitability as well as a depolarization of
the membrane and an increase in input resistance. Interestingly, with
the exception of the suppression of the mAHP, these effects were
persistent, and in the case of the sAHP lasting for more than 1 h
of drug washout. Preincubation with the specific mGluR5 antagonist,
2-methyl-6-(phenylethynyl)-pyridine (MPEP), reduced but did not
completely prevent the effects of DHPG. However, preincubation with
both MPEP and the mGluR1 antagonist LY367385 completely prevented the
DHPG-induced changes. These results demonstrate that the DHPG-induced
changes are mediated partly by mGluR5 and partly by mGluR1. Because
Group I mGluRs are linked to PLC via G-protein activation, we also
investigated pathways downstream of PLC activation, using chelerythrine
and cyclopiazonic acid to block protein kinase C (PKC) and inositol 1,4,5-trisphosphate-(IP3)-activated
Ca2+ stores, respectively. Neither inhibitor
affected the DHPG-induced suppression of the sAHP or the increase in
excitability nor did an inhibitor of PLC itself, U-73122. Taken
together, these results argue that in CA1 pyramidal cells in the adult
rat, DHPG activates mGluRs of both the mGluR5 and mGluR1 subtypes,
causing a long-lasting suppression of the sAHP and a consequent
persistent increase in excitability via a PLC-, PKC-, and
IP3-independent transduction pathway.
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