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Cerebral Cortex Advance Access published online on January 5, 2005
Cerebral Cortex, doi:10.1093/cercor/bhi022
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© Oxford University Press 2005; all rights reserved

Article

The Metabotropic Glutamate Receptor mGluR3 is Critically Required for Hippocampal Long-term Depression and Modulates Long-term Potentiation in the Dentate Gyrus of Freely Moving Rats

Beatrice Pöschel 1, Barbara Wroblewska 2, Uwe Heinemann 3, and Denise Manahan-Vaughan 1*

1 Learning and Memory Research, International Graduate School of Neuroscience, Ruhr University Bochum, Universitätsstr. 150, 44780 Bochum, Germany; Institute for Physiology of the Charite, Synaptic Plasticity Research, Humboldt University, Berlin, Germany
2 Georgetown University, Department of Biology, 37th & O Sts NW, Washington, DC 20057, USA
3 Institute for Physiology of the Charite, Department of Neurophysiology, Humboldt University, Berlin, Germany

* To whom correspondence should be addressed.
Denise Manahan-Vaughan, E-mail: vaughan{at}neurobiologie.rub.de


  Abstract

Group II metabotropic glutamate receptors (mGluRs) play an important role in the regulation of hippocampal synaptic plasticity in vivo: long-term potentiation (LTP) is inhibited and long-term depression (LTD) is enhanced by activation of these receptors. The contribution, in vivo, of the individual group II mGluR subtypes has not been characterized. We analysed the involvement of the subtype mGluR3 in LTD and LTP. Rats were implanted with electrodes to enable chronic measurement of evoked potentials from medial perforant path-dentate gyrus synapses. Neither the selective mGluR3 agonist, N-acetylaspartylglutamate (NAAG), nor the antagonist {beta}-NAAG, given intracerebrally, affected basal synaptic transmission. {beta}-NAAG significantly inhibited LTD expression. NAAG exhibited transient inhibitory effects on the intermediate phase of LTD. Whereas NAAG altered paired-pulse responses, {beta}-NAAG had no effect, suggesting that antagonism of mGluR3 prevents LTD via a postsynaptic mechanism, whereas agonist activation of mGluR3 modulates LTD at a presynaptic locus. NAAG impaired the expression of LTP, whereas {beta}-NAAG had no effect. NAAG effects on LTP were blocked by EGLU, a selective group II mGluR antagonist. Our data suggest an essential role for mGluR3 in LTD, and a modulatory role for mGluR3 in LTP, with effects being mediated by distinct pre- and post-synaptic loci.

Keywords: EGLU; NAAG; paired-pulse; perforant path; synaptic plasticity.
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