Willott J F, Milbrandt J C, Bross L S, Caspary D M
Department of Psychology, Northern Illinois University, DeKalb 60115, USA.
J Comp Neurol. 1997 Sep 1;385(3):405-14.
Glycinergic neurons in the cochlear nucleus (CN) of C57BL/6J (C57) and CBA/CaJ (CBA) mice were studied by using immunocytochemical and receptor-binding techniques. Adult C57 mice exhibit progressive cochlear pathology as they age, whereas aging CBA mice retain good hearing. In the CN of old C57 mice (18 months) with severe hearing loss, the number of glycine-immunoreactive neurons decreased significantly. The number (Bmax) of strychnine-sensitive glycine receptors (GlyR) decreased significantly in the dorsal CN of old C57 mice. Significant effects were not observed in the CN of middle-aged C57 mice (with less-severe hearing loss) or in very old CBA mice (which do not exhibit severe hearing loss). The data suggest that the combination of severe hearing loss and old age results in deficits in one or more inhibitory glycinergic circuits in the CN.
利用免疫细胞化学和受体结合技术，对C57BL/6J（C57）和CBA/CaJ（CBA）小鼠耳蜗核（CN）中的甘氨酸能神经元进行了研究。成年C57小鼠随着年龄增长会出现进行性耳蜗病理变化，而衰老的CBA小鼠听力保持良好。在患有严重听力损失的老年C57小鼠（18个月）的CN中，甘氨酸免疫反应性神经元的数量显著减少。老年C57小鼠背侧CN中士的宁敏感型甘氨酸受体（GlyR）的数量（Bmax）显著减少。在中年C57小鼠（听力损失较轻）的CN或非常老的CBA小鼠（未表现出严重听力损失）的CN中未观察到显著影响。数据表明，严重听力损失和老年相结合会导致CN中一个或多个抑制性甘氨酸能回路出现缺陷。
