Role of cochlear integrity in cochlear nucleus glucose metabolism and neuron number after cochlea removal in aging broiler chickens.
In the chicken auditory system, cochlear nucleus (nucleus magnocellularis, NM) neurons receive their only excitatory input from the ipsilateral cochlea. Cochlea removal (CR) results in an immediate decrease in NM neuron electrical activity, followed by death of approximately 30% of NM neurons. Previous work showed a decrease in NM activity and subsequent loss of NM neurons in all chicks. Egg layer adults showed NM neuron loss after CR, while neuron number remained stable in broiler adults. This suggested that effects of CR on NM were age- and breed-dependent. We now know that most aging egg layer chickens maintain largely normal cochleae throughout adulthood. Some exhibit cochlear damage with age. The converse is true of broiler chickens. Most aging broiler chickens display cochlear degeneration, with some maintaining normal cochlear anatomy throughout adulthood. The presence of extensive cochlear damage may alter the effect of CR on NM, leading to the described differences. Here, we examine the effect of unilateral CR on NM glucose metabolism and neuron number in 2, 30, 39, and 52 week-old broiler chickens found to have normal cochleae. Chickens with damaged cochleae were excluded. Using 2-deoxyglucose uptake to evaluate bilateral NM glucose metabolism, we found significantly decreased uptake ipsilateral to CR at each age examined. Bilateral cell counts revealed significant neuron loss ipsilateral to CR at each age examined. This suggests that NM glucose metabolism decreases and subsequent neuron death occurs in aging broiler chickens when a normal cochlea is removed. The status of the cochlea must play a role in the effect of deafferentation on NM glucose metabolism and neuron survival. The effect of CR appears to be dependent upon neither age nor breed, but upon cochlear integrity instead.
Smittkamp
Susan E
SE
Department of Hearing and Speech, Smith Mental Retardation Research Center, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Girod
Douglas A
DA
Durham
Dianne
D
D000375:Aging / Q000378:metabolism / Q000502:physiology*; D000704:Analysis of Variance; D000818:Animals; D002452:Cell Count; D016923:Cell Death / Q000502:physiology; D002645:Chickens; D003051:Cochlea / Q000473:pathology / Q000502:physiology* / Q000648:ultrastructure; D017626:Cochlear Nucleus / Q000378:metabolism* / Q000473:pathology; D003847:Deoxyglucose / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006198:Hair Cells, Auditory / Q000473:pathology / Q000502:physiology / Q000648:ultrastructure; D008855:Microscopy, Electron, Scanning; D009475:Neurons, Afferent / Q000166:cytology / Q000378:metabolism*
D003847:Deoxyglucose; D005947:Glucose