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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 m Glu R2, a metabotropic glutamate receptor, in the AOB and the fact that the activation of m Glu R2 permits the formation of a specific olfactory memory, we reasoned that m Glu R2 might play an important role in regulating dendrodendritic inhibition. To test this hypothesis, we examined the effects of pharmacological and genetic manipulations of m Glu R2 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 m V 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 ( mGlu R2/ mGluR3), DCG- IV [(2 S,1′ R,2′ R,3′ R)-2-(2,3-dicarboxycyclopropyl)glycine], suppressed, whereas the m GluR2/m Glu R3 antagonist LY341495 [(αS)-α-amino-α-[(1S,2S)-2-carboxycyclopropyl]-9H-xanthine-9-propanoic acid] enhanced dendrodendritic inhibition. Genetic ablation of mGlu R2 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 m GluR2 reduces dendrodendritic inhibition by inhibiting synaptic transmission between mitral cells and granule cells in the AOB. [ABSTRACT FROM AUTHOR]