PMID- 23167899 OWN - NLM STAT- MEDLINE DCOM- 20130715 LR - 20131121 IS - 1460-9568 (Electronic) IS - 0953-816X (Linking) VI - 37 IP - 3 DP - 2013 Feb TI - Regulation of synaptic currents by mGluR2 at reciprocal synapses in the mouse accessory olfactory bulb. PG - 351-8 LID - 10.1111/ejn.12059 [doi] AB - The throughput of information from the accessory olfactory bulb (AOB) to downstream structures is controlled by reciprocal dendrodendritic inhibition of mitral cells by granule cells. Given the high expression levels of mGluR2, a metabotropic glutamate receptor, in the AOB and the fact that the activation of mGluR2 permits the formation of a specific olfactory memory, we reasoned that mGluR2 might play an important role in regulating dendrodendritic inhibition. To test this hypothesis, we examined the effects of pharmacological and genetic manipulations of mGluR2 on synaptic responses measured from mitral or granule cells in slice preparations from 23- to 36-day-old Balb/c mice. To evoke dendrodendritic inhibition, a depolarizing voltage step from -70 to 0 mV or a threshold current stimulus adjusted to elicit action potential(s) was applied to a mitral cell using either a nystatin-perforated or conventional whole-cell configuration. We found that an agonist for group II metabotropic glutamate receptors (mGluR2/mGluR3), DCG-IV [(2S,1'R,2'R,3'R)-2-(2,3-dicarboxycyclopropyl)glycine], suppressed, whereas the mGluR2/mGluR3 antagonist LY341495 [(alphaS)-alpha-amino-alpha-[(1S,2S)-2-carboxycyclopropyl]-9H-xanthine-9-propanoic acid] enhanced dendrodendritic inhibition. Genetic ablation of mGluR2 markedly impaired the effects of DCG-IV and LY341495 on dendrodendritic inhibition. DCG-IV reduced both the frequency and the amplitude of spontaneous miniature excitatory postsynaptic currents recorded from granule cells. Additionally, DCG-IV inhibited high-voltage-activated calcium currents in both mitral and granule cells. These results suggest that mGluR2 reduces dendrodendritic inhibition by inhibiting synaptic transmission between mitral cells and granule cells in the AOB. CI - (c) 2012 Federation of European Neuroscience Societies and Blackwell Publishing Ltd. FAU - Taniguchi, Mutsuo AU - Taniguchi M AD - Department of Physiology, Kochi Medical School, Nankoku, Japan. tanigucm@kochi-u.ac.jp FAU - Yokoi, Mineto AU - Yokoi M FAU - Shinohara, Yoshiaki AU - Shinohara Y FAU - Okutani, Fumino AU - Okutani F FAU - Murata, Yoshihiro AU - Murata Y FAU - Nakanishi, Shigetada AU - Nakanishi S FAU - Kaba, Hideto AU - Kaba H LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20121121 PL - France TA - Eur J Neurosci JT - The European journal of neuroscience JID - 8918110 RN - 0 (Amino Acids) RN - 0 (Anticonvulsants) RN - 0 (Calcium Channels) RN - 0 (Cyclopropanes) RN - 0 (Excitatory Amino Acid Antagonists) RN - 0 (LY 341495) RN - 0 (Receptors, Metabotropic Glutamate) RN - 0 (Xanthenes) RN - 0 (metabotropic glutamate receptor 2) RN - 147782-19-2 (2-(2,3-dicarboxycyclopropyl)glycine) RN - TE7660XO1C (Glycine) SB - IM MH - Action Potentials MH - Amino Acids/pharmacology MH - Animals MH - Anticonvulsants/pharmacology MH - Calcium Channels/drug effects/metabolism MH - Cyclopropanes/pharmacology MH - Dendrites/metabolism/physiology MH - Excitatory Amino Acid Antagonists/pharmacology MH - *Excitatory Postsynaptic Potentials MH - Glycine/analogs & derivatives/pharmacology MH - Mice MH - Mice, Inbred BALB C MH - Mutation MH - Olfactory Bulb/cytology/metabolism/*physiology MH - Receptors, Metabotropic Glutamate/agonists/antagonists & inhibitors/genetics/*metabolism MH - Synapses/metabolism/*physiology MH - Xanthenes/pharmacology EDAT- 2012/11/22 06:00 MHDA- 2013/07/17 06:00 CRDT- 2012/11/22 06:00 PHST- 2012/10/02 00:00 [received] PHST- 2012/10/16 00:00 [accepted] PHST- 2012/11/22 06:00 [entrez] PHST- 2012/11/22 06:00 [pubmed] PHST- 2013/07/17 06:00 [medline] AID - 10.1111/ejn.12059 [doi] PST - ppublish SO - Eur J Neurosci. 2013 Feb;37(3):351-8. doi: 10.1111/ejn.12059. Epub 2012 Nov 21.