Webster M, Webster D B
Brain Res. 1981 May 11;212(1):17-30. doi: 10.1016/0006-8993(81)90028-7.
The packing density of spiral ganglion neurons was measured in 2.5- and 13-15-month-old guinea pigs, in guinea pigs at various times after drug-deafening or acoustic trauma, and in Waltzing guinea pigs of various ages. Analysis of variance and Duncan's new multiple range tests were used to determine significant differences between treatment/survival groups. Spiral ganglion neurons in young and old normal ears did not have significantly different packing densities. Drug-deaf guinea pigs showed a significant loss of neurons by 2 weeks following treatment, a further significant loss by 2 months, and a marginally significant loss between 4 and 8 months. The neuronal population was then stable through 15 months, at about 13% of normal. Acoustic trauma ears showed the first significant loss isn the lower second turn at 1 month. Long-term (12-14 months post-exposure) trauma ears were highly variable. Waltzers lost about 50% of their normal neuronal population between 4 and 8 months; they showed an unexpected greater-than-normal density at 2 months, possible explanations of which are discussed. Thus, loss of the organ of Corti from various causes results in a slow but progressive loss of spiral ganglion neurons, the time course of which varies with the type of cochlear insult.
在2.5月龄和13 - 15月龄的豚鼠、药物致聋或声创伤后不同时间点的豚鼠以及不同年龄的华尔兹豚鼠中测量螺旋神经节神经元的堆积密度。采用方差分析和邓肯新复极差检验来确定治疗/存活组之间的显著差异。正常年轻和老年耳朵中的螺旋神经节神经元堆积密度没有显著差异。药物致聋的豚鼠在治疗后2周显示神经元显著丢失，2个月时进一步显著丢失，4至8个月之间有轻微显著丢失。然后神经元数量在15个月内保持稳定，约为正常水平的13%。声创伤耳朵在1个月时在较低的第二圈显示出首次显著丢失。长期（暴露后12 - 14个月）创伤耳朵差异很大。华尔兹豚鼠在4至8个月之间失去了约50%的正常神经元数量；它们在2个月时显示出意外高于正常的密度，并对其可能的解释进行了讨论。因此，各种原因导致的柯蒂氏器丧失会导致螺旋神经节神经元缓慢但渐进性的丢失，其时间进程因耳蜗损伤类型而异。
