Regulation of synaptic currents by m G lu R 2 at reciprocal synapses in the mouse accessory olfactory bulb

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 G lu R 2, a metabotropic glutamate receptor, in the AOB and the fact that the activation of m G lu R 2 permits the formation of a specific olfactory memory, we reasoned that m G lu R 2 might play an important role in regulating dendrodendritic inhibition. To test this hypothesis, we examined the effects of pharmacological and genetic manipulations of m G lu R 2 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 ( mG lu R 2/ mG luR3), DCG ‐ IV [(2 S ,1′ R ,2′ R ,3′ R )‐2‐(2,3‐dicarboxycyclopropyl)glycine], suppressed, whereas the m G luR2/m G lu R 3 antagonist LY341495 [(αS)‐α‐amino‐α‐[(1S,2S)‐2‐carboxycyclopropyl]‐9H‐xanthine‐9‐propanoic acid] enhanced dendrodendritic inhibition. Genetic ablation of mG lu R 2 markedly impaired the effects of DCG ‐ IV and LY 341495 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 G luR2 reduces dendrodendritic inhibition by inhibiting synaptic transmission between mitral cells and granule cells in the AOB .