Wiegand S J, Terasawa E
Neuroendocrinology. 1982 Jun;34(6):395-404. doi: 10.1159/000123335.
The present study examines the function of several cytologically distinct suprachiasmatic structures in the regulation of ovulation and positive feedback effects of estrogen and progesterone on gonadotropin release in the rat. Small (0.6-0.8 mm dia.) electrolytic lesions were placed at four loci along the rostrocaudal extent of the suprachiasmatic region in regularly cycling female rats. Anovulatory persistent estrus occurred only when lesions were located either in the suprachiasmatic nucleus (SCN) or the medial preoptic nucleus (MPN), a small periventricular cell group lying immediately caudal to the organum vasculosum lamina terminalis (OVLT). Lesions restricted to the OVLT and adjacent ventral prechiasmatic region (VPC-L), or the anterior suprachiasmatic region (ASR) between the MPN and SCN resulted in irregular estrous cycles frequently marked by periods of prolonged diestrus. Following administration of 50 microgram estradiol benzoate (EB) a daily afternoon surge of gonadotropin was observed in control animals. This circadian release of gonadotropins was completely abolished by SCN, ASR and MPN lesions. EB-induced gonadotropin surges were also greatly attenuated by VPC-L lesions. Subsequent administration of 1.5 mg progesterone (P) induced large surges of luteinizing hormone and follicle-stimulating hormone in VPC-L and ASR lesioned animals as well as controls. P administration also elicited gonadotropin surges in SCN lesioned animals, although surges were markedly attenuated in magnitude compared to controls. Only lesions that destroyed the MPN and immediately adjacent periventricular tissue completely and invariably eliminated P-induced gonadotropin release. Thus, anovulatory-persistent estrus appears to be associated specifically with lesions that interfere with the-positive feedback effect of P (MPN and SCN lesions). Animals with lesions that block or attenuate EB effects without interfering with P sensitive neural substrates can maintain long-term spontaneous ovulation (VPC-L and ASR lesions). An hypothesis is advanced to account for the differential effect of MPN and SCN lesions on P-induced gonadotropin release.
本研究探讨了大鼠视交叉上核中几个细胞结构不同的区域在排卵调节以及雌激素和孕酮对促性腺激素释放的正反馈作用中的功能。在处于正常发情周期的雌性大鼠的视交叉上核区域，沿前后方向的四个位点进行了直径为0.6 - 0.8毫米的电解损伤。只有当损伤位于视交叉上核（SCN）或内侧视前核（MPN）时，才会出现无排卵的持续发情，MPN是位于终板血管器（OVLT）尾侧紧邻的一个小室周细胞群。局限于OVLT及其相邻腹侧视交叉前区（VPC-L）或MPN与SCN之间的视交叉上前区（ASR）的损伤会导致发情周期不规则，常以长时间的间情期为特征。给对照动物注射50微克苯甲酸雌二醇（EB）后，每天下午观察到促性腺激素的激增。SCN、ASR和MPN损伤完全消除了这种促性腺激素的昼夜节律释放。VPC-L损伤也大大减弱了EB诱导的促性腺激素激增。随后给VPC-L和ASR损伤的动物以及对照动物注射1.5毫克孕酮（P），诱导出大量的促黄体生成素和促卵泡激素激增。给SCN损伤的动物注射P也会引发促性腺激素激增，尽管与对照相比，激增幅度明显减弱。只有完全破坏MPN及其紧邻的室周组织的损伤才会完全且始终消除P诱导的促性腺激素释放。因此，无排卵的持续发情似乎与干扰P正反馈作用的损伤（MPN和SCN损伤）特别相关。那些损伤阻断或减弱EB作用但不干扰P敏感神经基质的动物能够维持长期自发排卵（VPC-L和ASR损伤）。本文提出了一个假说，以解释MPN和SCN损伤对P诱导的促性腺激素释放的不同影响。
