Kohama S G, Brown S A, Finch C E, McNeill T H
Neurogerontology Division, University of Southern California, Los Angeles 90089-0191.
Brain Res. 1992 Mar 6;574(1-2):341-4. doi: 10.1016/0006-8993(92)90838-z.
Age-related decline in estrous cycle frequency and impaired pre-ovulatory gonadotropin surges at mid-life are modelled in young C57BL/6J mice by chronic (3 months) oral administration of estradiol (E2). However, the cellular events that induce damage to the neuroendocrine center that regulate gonadotropins with age or following E2 treatment are unclear. To address this issue, possible neuron loss was examined in relation to the loss of estrous cyclicity in E2-treated mice, in particular neurons of the hypothalamic luteinizing hormone releasing hormone (LHRH) and/or tuberoinfundibular dopaminergic (TIDA) systems. By immunocytochemical methods, there was no change in the number of LHRH or TIDA neurons in mice that have become acyclic due to age or E2 treatment. We conclude that the onset of acyclicity at middle-age or following chronic E2 treatment is not associated with loss of LHRH or TIDA neurons and that other neuroendocrine changes must be considered for the cause of acyclicity, particularly those involved in the synaptic regulation of LHRH secretion.
通过对年轻的C57BL/6J小鼠进行为期3个月的雌二醇（E2）慢性口服给药，模拟中年时与年龄相关的发情周期频率下降以及排卵前促性腺激素激增受损的情况。然而，随着年龄增长或E2治疗后，导致调节促性腺激素的神经内分泌中心受损的细胞事件尚不清楚。为了解决这个问题，研究了E2处理小鼠中与发情周期丧失相关的可能的神经元丢失情况，特别是下丘脑促黄体生成素释放激素（LHRH）和/或结节漏斗多巴胺能（TIDA）系统的神经元。通过免疫细胞化学方法，发现因年龄增长或E2处理而出现无发情周期的小鼠中，LHRH或TIDA神经元的数量没有变化。我们得出结论，中年时或慢性E2治疗后无发情周期的开始与LHRH或TIDA神经元的丢失无关，并且必须考虑其他神经内分泌变化作为无发情周期的原因，特别是那些参与LHRH分泌突触调节的变化。
