Recurrent dendrodendritic inhibition of accessory olfactory bulb mitral cells requires activation of group I metabotropic glutamate receptors

Metabotropic glutamate receptors ( mGluRs) modulate neural excitability and network tone in many brain regions. Expression of mGluRs is particularly high in the accessory olfactory bulb ( AOB), a CNS structure critical for detecting chemicals that identify kin and conspecifics. Because of its relative simplicity and its direct projection to the hypothalamus, the AOB provides a model system for studying how mGluRs affect the flow of encoded sensory information to downstream areas. We investigated the role of group I mGluRs in synaptic processing in AOB slices and found that under control conditions, recurrent inhibition of principal neurons ( mitral cells) was completely eliminated by the mGluR1 antagonist LY367385 [( S)-( +)-alpha-amino-4-carboxy-2methylbenzeneacetic acid]. In addition, the group I mGluR agonist DHPG [( S)-3,5-dihydroxyphenylglycine; 20 mu M] induced a dramatic increase in the rate of spontaneous IPSCs. This increase was dependent on voltage-gated calcium channels but persisted even after blockade of ionotropic glutamatergic transmission and sodium channels. Together, these results indicate that mGluR1 plays a critical role in controlling information flow through the AOB and suggest that mGluR1 may be an important locus for experience-dependent changes in synaptic function.