Transneuronal regulation of ribosomes after blockade of ionotropic excitatory amino acid receptors.

Elimination of auditory nerve activity results in death and atrophy of neurons in the cochlear nucleus, nucleus magnocellularis (NM), of the chick. One early event believed to lead to cell death and atrophy is the disruption of ribosomes in the NM neuron. A useful assay for visualizing these ribosomal changes is immunolabeling with the antibody Y10B, which recognizes ribosomal RNA. Activity-dependent changes in Y10B labeling have been observed both in vivo, after unilateral cochlea removal and in vitro after unilateral auditory nerve stimulation. Although it is clear that activity is crucial for maintaining ribosomal integrity, the identity of the important transynaptic signal(s) is not known. It is possible that this trophic signal is glutamate, the neurotransmitter release from the auditory nerve. The present study investigates the role of ionotropic glutamate receptors in the activity-dependent regulation of ribosomes, as measured by the Y10B immunoreactivity. Brain slices containing the auditory nerve and NM on both sides were obtained from hatchling chicks. The auditory nerve on one side of the slice was stimulated for 1 h. The slice was then processed for Y10B immunoreactivity. As expected, greater Y10B immunolabeling was observed on the stimulated side of the slice. Unexpectedly, however, this immunolabeling difference was still observed after blocking NMDA receptors (50 microM DL-APV), non-NMDA receptors (20 microM CNQX), or blocking both ionotropic receptor subtypes (APV and CNQX). This was true even though CNQX eliminated driven postsynaptic potentials. These data suggest that ionotropic glutamate receptors are not necessary for the activity-dependent regulation of ribosomes in NM neurons.