title: Regulation of synaptic currents by mGluR2 at reciprocal synapses in the mouse accessory olfactory bulb.
abstract: 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 [(αS)-α-amino-α-[(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.
authors.affiliation: Department of Physiology, Kochi Medical School, Nankoku, Japan. tanigucm@kochi-u.ac.jp
authors.forename: Mutsuo
authors.initials: M
authors.lastname: Taniguchi
authors.forename: Mineto
authors.initials: M
authors.lastname: Yokoi
authors.forename: Yoshiaki
authors.initials: Y
authors.lastname: Shinohara
authors.forename: Fumino
authors.initials: F
authors.lastname: Okutani
authors.forename: Yoshihiro
authors.initials: Y
authors.lastname: Murata
authors.forename: Shigetada
authors.initials: S
authors.lastname: Nakanishi
authors.forename: Hideto
authors.initials: H
authors.lastname: Kaba
mesh_terms: D000200:Action Potentials; D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology; D015220:Calcium Channels / Q000187:drug effects / Q000378:metabolism; D003521:Cyclopropanes / Q000494:pharmacology; D003712:Dendrites / Q000378:metabolism / Q000502:physiology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D019706:Excitatory Postsynaptic Potentials; D005998:Glycine / Q000031:analogs & derivatives / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D009154:Mutation; D009830:Olfactory Bulb / Q000166:cytology / Q000378:metabolism / Q000502:physiology*; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D013569:Synapses / Q000378:metabolism / Q000502:physiology*; D014966:Xanthenes / Q000494:pharmacology
chemical_list: D000596:Amino Acids; D000927:Anticonvulsants; D015220:Calcium Channels; D003521:Cyclopropanes; D018691:Excitatory Amino Acid Antagonists; C114624:LY 341495; D018094:Receptors, Metabotropic Glutamate; D014966:Xanthenes; C108822:metabotropic glutamate receptor 2; C082313:2-(2,3-dicarboxycyclopropyl)glycine; D005998:Glycine