mGluRs modulate neuronal firing in the auditory midbrain

The mechanisms underlying sound-evoked suppression of neuronal firing in the auditory system are poorly understood. To explore these mechanisms in the inferior colliculus (IC), agonists and antagonists targeting different groups of metabotropic glutamate receptors (mGluRs) were applied iontophoretically to IC neurons in awake mice. We found that a group I-specific mGluR agonist predominantly increased neuronal firing in 52% of neurons, whereas group I antagonist had the opposite effect in 51% of neurons. A group II specific agonist showed no effect on neuronal firing but an antagonist increased firing rate in 48% of neurons. Neither a group III-specific mGluR agonist nor an antagonist had an effect on neuronal firing in the IC. We also found that sound stimuli triggered suppression of spontaneous firing in 70% of IC neurons. This suppression was reversibly blocked by group I mGluR antagonists. There is a possible link between this suppression and two perceptual phenomena: forward masking and "residual inhibition," the brief reduction/elimination of tinnitus following an appropriate masking sound.