Hayashi S, Aihara M, Wakabayashi K
Department of Anatomy and Embryology, Tokyo Metropolitan Institute for Neurosciences, Japan.
Neurosci Res. 1991 Oct;12(2):366-78. doi: 10.1016/0168-0102(91)90004-i.
The rostro-caudal distribution of luteinizing hormone-releasing hormone (LHRH) in the hypothalamus of neonatally estrogenized (10 micrograms EB for 1-5 days), sterile female rats was compared with that of cycling rats at 50, 100 and 240 days of age. Serial slices of 400 microns in thickness in total were cut from a hypothalamic block, and the LHRH content of each slice was measured by radioimmunoassay. Two peaks of LHRH in the rostro-caudal direction were apparent in all groups. The rostral peak corresponded to the LHRH-producing cells in the septal-preoptic region and storage of LHRH in the organum vasculosum lamina terminalis (OVLT), while the caudal peak corresponded to that of LHRH in the median eminence. Thus, the total LHRH content of the regions of the hypothalamus was calculated separately either anterior or posterior to the suprachiasmatic nucleus, which were designated as the rostral hypothalamus (RH) and mediobasal hypothalamus (MBH), respectively. The total content of LHRH in the 50-day-old sterile rats was significantly higher than that in the estrous females in both RH and MBH. This was also true for the MBH of 240-day-old sterile females in comparison to that of estrous females but not so in 100-day-old females. The present results suggest that sterility in neonatally estrogenized rats is not due to a reduction in LHRH content of the hypothalamus but, rather, is due to changes in LHRH-releasing systems. Furthermore, in the control females, ovariectomy performed at 22 days of age induced a striking decrease in LHRH content in the MBH at 50 days of age, while it remained unchanged after ovariectomy in the neonatally estrogenized sterile rats. These findings suggest that the hypothalamic mechanism involved in the release of LHRH after ovariectomy was damaged by neonatal treatment with estrogen.
将新生期经雌激素处理(1 - 5天给予10微克雌二醇)的无菌雌性大鼠下丘脑促黄体生成激素释放激素(LHRH)的头尾分布,与50、100和240日龄的性周期正常大鼠进行比较。从下丘脑块切取总厚度为400微米的连续切片,通过放射免疫测定法测量每片的LHRH含量。在所有组中,LHRH在头尾方向上均有两个明显的峰值。头侧峰值对应于隔区 - 视前区产生LHRH的细胞以及终板血管器(OVLT)中LHRH的储存,而尾侧峰值对应于正中隆起处的LHRH峰值。因此,分别计算视交叉上核之前或之后下丘脑区域的总LHRH含量,分别将其指定为下丘脑前部(RH)和下丘脑中间基底部(MBH)。50日龄无菌大鼠的RH和MBH中LHRH的总含量均显著高于发情期雌性大鼠。与发情期雌性大鼠相比,240日龄无菌雌性大鼠的MBH中也是如此,但100日龄雌性大鼠并非如此。目前的结果表明,新生期经雌激素处理的大鼠不育并非由于下丘脑LHRH含量降低,而是由于LHRH释放系统的变化。此外,在对照雌性大鼠中,22日龄时进行卵巢切除术会导致50日龄时MBH中LHRH含量显著降低,而新生期经雌激素处理的无菌大鼠在卵巢切除术后LHRH含量保持不变。这些发现表明,卵巢切除术后参与LHRH释放的下丘脑机制因新生期雌激素处理而受损。