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ISSN : 1226-7155(Print)
ISSN : 2287-6618(Online)
International Journal of Oral Biology Vol.36 No.2 pp.71-78

Roles of Metabotropic Glutamate Receptors 1 and 5 in Rat Medial Vestibular Nucleus Neurons

Sang Woo Chun, Hae In Lee, Sung Hyo Lee
Dept. of Oral Physiology, College of Dentistry, Institute of Wonkwang Biomaterial and Implant, Wonkwang University
(received March 18, 2011 ; revised April 19, 2011 ; accepted April 22, 2011)


Using whole cell current- and voltage-clamp recording weinvestigated the characteristics and pharmacology of group Imetabotropic glutamate receptor (mGluR)-mediated responsesin rat medial vestibular nucleus (MVN) neurons. Incurrent clamp conditions, activation of mGluR I by applicationof the group I mGluR agonist (R,S)-3,5-dihydroxyphenylglycine(DHPG) induced a direct excitation of MVNneurons that is characterized by depolarization and increasedspontaneous firing frequency. To identify which of mGluRsubtypes are responsible for the various actions of DHPG inMVN, we used two subtype-selective antagonists. (S)-(+)-alpha-amino-a-methylbenzeneacetic acid (LY367385) is apotent competitive antagonist that is selective for mGluR1,whereas 2-methyl-6-(phenylethynyl)-pyridine (MPEP) is apotent noncompetitive antagonist that is selective formGluR5. In voltage clamp conditions, DHPG applicationincreased the frequency of spontaneous and miniature inhibitorypostsynaptic currents (IPSCs) but had no effect onamplitude distributions. Antagonism of the DHPG-inducedincrease of miniature IPSCs required the blockade of bothmGluR1 and mGluR5. DHPG application induced an inwardcurrent, which can be enhanced under depolarized conditions.DHPG-induced current was blocked by LY367385,but not by MPEP. Both LY367385 and MPEP antagonizedthe DHPG-induced suppression of the calciumactivatedpotassium current (IAHP). These data suggest that mGluR1and mGluR5 have similar roles in the regulation of theexcitability of MVN neurons, and show a little distinct.Furthermore, mGluR I, via pre- and postsynaptic actions,have the potential to modulate the functions of the MVN.