ABSTRACT
Elimination of eighth-nerve activity results in the death of 30% of the neurons in the chick cochlear nucleus, nucleus magnocellularis (NM). One early event in this cell death cascade is the disruption of ribosomes in NM neurons which can be observed within 1 h following deafferentation. These rapid changes in ribosomes can be visualized using Y10B, a monoclonal antibody that recognizes ribosomal RNA. Previous studies using a brain slice preparation of the avian brain stem auditory system have shown that activation of metabotropic glutamate receptors (mGluRs) is necessary for the activity-dependent maintenance of Y10B antigenicity. The purpose of the present study was to determine if group I and/or II mGluRs are necessary for this activity-dependent regulation. This was accomplished by selectively blocking group I or II receptors while unilaterally stimulating the auditory nerve in vitro. In normal media, unilateral stimulation of the auditory nerve resulted in darker Y10B immunolabeling of NM neurons on the stimulated side of the slice. The group I antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid (AIDA) and the group II antagonists LY341495 and (S)-alpha-ethylglutamic acid (EGLU) all prevented the activity-dependent difference in Y10B immunolabeling. These data suggest that both group I and II mGluRs play vital roles in the activity-dependent regulation of ribosomes in NM.
