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 removing auditory nerve stimulation of NM, intracellular calcium concentration ([Ca2+]i) rises by up to 400% while the integrity of ribosomes begins to decline. High levels of excess Ca2+ in cells are toxic and may be a cause of cell death in NM, as well as lead to ribosome dysfunction through Ca2+ signaling mechanisms. Glutamate-releasing axons of the auditory nerve have been shown to maintain NM neuron health by activating group I and II metabotropic glutamate receptors (mGluRs), preventing Ca2+ increases and maintaining ribosomal integrity. This study aims to determine how [Ca2+]i and ribosomal integrity are maintained by auditory nerve stimulation by selectively blocking mGluR subtypes during stimulation. The abundance of Ca2+ in NM neurons was quantified using in vitro ratiometric calcium imaging, while ribosomal integrity was assayed in the same tissue slices using Y10B immunolabeling. It was expected that group I and group II mGluRs act on independent mechanisms to control both calcium and ribosome homeostasis. So far, blockade of both groups of mGluRs have led to ribosome integrity changes, but surprisingly only group I blockade results in increased [Ca2+]i. These preliminary results suggest dissociation in how calcium and ribosomes are regulated in NM neurons.
