Smittkamp Susan E, Girod Douglas A, Durham Dianne
Department of Hearing and Speech, Smith Mental Retardation Research Center, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Hear Res. 2005 Jun;204(1-2):48-59. doi: 10.1016/j.heares.2004.12.011.
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.
在鸡的听觉系统中，蜗神经核（巨细胞神经核，NM）神经元仅从同侧耳蜗接受兴奋性输入。切除耳蜗（CR）会导致NM神经元电活动立即下降，随后约30%的NM神经元死亡。先前的研究表明，所有雏鸡的NM活动都会下降，随后NM神经元会丢失。蛋鸡成年后CR会导致NM神经元丢失，而肉鸡成年后神经元数量保持稳定。这表明CR对NM的影响取决于年龄和品种。我们现在知道，大多数老龄蛋鸡在成年期耳蜗基本保持正常。有些随着年龄增长会出现耳蜗损伤。肉鸡则相反。大多数老龄肉鸡表现出耳蜗退化，有些在成年期耳蜗解剖结构保持正常。广泛的耳蜗损伤可能会改变CR对NM的影响，导致上述差异。在这里，我们研究了单侧CR对2周龄、30周龄、39周龄和52周龄耳蜗正常的肉鸡NM葡萄糖代谢和神经元数量的影响。耳蜗受损的鸡被排除在外。利用2-脱氧葡萄糖摄取来评估双侧NM葡萄糖代谢，我们发现在每个检查年龄，CR同侧的摄取量均显著下降。双侧细胞计数显示，在每个检查年龄，CR同侧均有显著的神经元丢失。这表明，在老龄肉鸡中，切除正常耳蜗会导致NM葡萄糖代谢下降以及随后的神经元死亡。耳蜗的状态必定在去传入对NM葡萄糖代谢和神经元存活的影响中起作用。CR的影响似乎既不取决于年龄也不取决于品种，而是取决于耳蜗的完整性。
