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Cochlea removal results in the death of 20-30% of neurons in nucleus magnocellularis (NM), a cochlear nucleus of the chick auditory system involved in the precise time-coding of acoustic signals. Within 1 hr of deafferentation, intracellular calcium concentration ([Ca2+]i) rises by up to 400% while the integrity of ribosomes begins to decline—two potentially cytotoxic events. Glutamatergic axons of the auditory nerve have been shown to maintain NM neuron health by activating group I and II metabotropic glutamate receptors (mGluRs), maintaining normal [Ca2+]i and ribosomal integrity. This study aimed to determine how [Ca2+]i and ribosomal integrity are maintained by auditory nerve stimulation by selectively blocking group I mGluRs with AIDA and group II mGluRs with LY 341495 during unilateral auditory nerve stimulation. The abundance of Ca2+ in NM neurons was quantified using in vitro fura-2 ratiometric calcium imaging, while ribosomal integrity was assayed in a subset of the same tissue slices using Y10B immunolabeling (Y10B-ir). It was expected that AIDA and LY 341495 would increase [Ca2+]i and these increases would occur in parallel with an elimination in stimulation-induced differences in Y10B-ir between stimulated and unstimulated neurons of a slice. AIDA caused large increases in [Ca2+]i and eliminated differences in Y10B-ir between sides. Surprisingly, LY 341495 failed to cause reliable increases in [Ca2+]i compared to stimulated controls, but still eliminated differences in Y10B-ir between sides. These results suggest dissociation in how calcium and ribosomes are regulated in NM neurons.