Effect of cochlear integrity on cochlear nucleus neuron glucose metabolism in aged adult broiler chickens

Abrupt removal of excitatory input is devastating to post-synaptic neurons in normally functioning sensory systems. In both mammalian and avian auditory systems, abrupt temporary or permanent experimental deafferentation stimulates a cascade of changes in central auditory structures that can result in neuron death. Effects of naturally occurring progressive deafferentation on central auditory structure and function have not been fully described. Extensive naturally occurring cochlear damage is found in some aged chickens, despite their regenerative capacity, providing the opportunity to examine the effects of this type of deafferentation on the avian cochlear nucleus (nucleus magnocellularis, NM). Previous evaluation of NM oxidative metabolism using cytochrome oxidase histochemistry revealed that naturally occurring cochlear damage results in down-regulated metabolism in corresponding regions of NM. It is unknown how progressive hair cell damage and loss affects NM glucose uptake. Here, NM glucose metabolism is assessed using 2-deoxyglucose uptake as a marker for metabolic activity in the presence of normal, mildly damaged, severely damaged, and totally damaged cochlear hair cells. Results indicate that while severe and total cochlear damage significantly decrease NM oxidative metabolism, only total damage results in significantly decreased NM glucose metabolism. Results are discussed in the context of functional reorganization and trophic support.