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Letters to Nature
Nature 366, 687-690 (16 December 1993) | doi:10.1038/366687a0; Accepted 6 October 1993
Role of a metabotropic glutamate receptor in synaptic modulation in the accessory olfactory bulb
Yasunori Hayashi*†,
Akiko Momiyama‡,
Tomoyuki Takahashi‡§,
Hitoshi Ohishi
,
Reiko Ogawa-Meguro
,
Ryuichi Shigemoto
,
Noboru Mizuno
&
Shigetada Nakanishi*¶
-
*, Institute for Immunology,†, Department of Pharmacology, ‡, Department of Physiology,
Department of Morphological Brain Science, Kyoto University Faculty of Medicine, Kyoto 606, Japan - § Present address: Department of Neurophysiology, Institute for Brain Research, Faculty of Medicine, University of Tokyo, Tokyo 113, Japan.
- ¶ To whom correspondence should be addressed.
Abstract
VARIOUS functions of glutamate transmission are mediated by both ionotropic and metabotropic glutamate receptors1. The metabotropic glutamate receptors (mGluRs) consist of at least six different subtypes that are classified into three subgroups, mGluR1/mGluR5, mGluR2/mGluR3, and mGluR4/mGluR6 (refs 1-5), but their physiological roles are largely unknown. Here we report the identification of a very potent agonist for mGluR2/mGluR3, DCG-IV, and the specific localization of mGluR2 in granule cell dendrites that form dendrodendritic synapses with mitral cells in the accessory olfactory bulb. Using the DCG-IV agonist for mGluR2 in combination with slice patch-recording, we demonstrate that the granule cell mGluR2 presynaptically suppresses inhibitory GABA (
-aminobutyrate) transmission to the mitral cell. Our results indicate that mGluR2 in granule cells plays an important role in the persistent excitation of olfactory sensory transmission in the accessory olfactory bulb by relieving mitral cells from the GABA inhibition.
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