Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9436578 | Hearing Research | 2005 | 13 Pages |
Abstract
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.
Keywords
Trk BPBSIACUCNIDCDPLSDNT4Tyrosine kinase receptor BNOF2-DeoxyglucoseGAP-43NT32DGDPOAEBDNFDistortion product otoacoustic emissionsanalysis of varianceANOVAprotected least significant differencegrowth associated protein-43Institutional Animal Care and Use CommitteeAgingcytochrome oxidaseAuditorybrain derived neurotrophic factorneurite outgrowth factorPhosphate buffered salineSEMChickenScanning electron microscopyNeurotrophin 3Neurotrophin 4nucleus magnocellularisoptical density
Related Topics
Life Sciences
Neuroscience
Sensory Systems
Authors
Susan E. Smittkamp, Dianne Durham,