Palm I F, Van Der Beek E M, Wiegant V M, Buijs R M, Kalsbeek A
The Netherlands Institute for Brain Research, Amsterdam.
Neuroscience. 1999;93(2):659-66. doi: 10.1016/s0306-4522(99)00106-2.
The luteinizing hormone surge in the female rat is the result of the integration of multiple signals within the medial preoptic area. The medial preoptic area contains gonadotropin-releasing hormone neurons that are responsible for the release of luteinizing hormone, neurons containing estrogen receptors and terminals originating from the suprachiasmatic nucleus with, for example, vasopressin as neurotransmitter. Both the medial preoptic area and suprachiasmatic nucleus are crucial for the occurrence of luteinizing hormone surges, since lesioning of either nucleus prevents pre-ovulatory and steroid-induced luteinizing hormone surges. In this study, we investigated whether vasopressin in the medial preoptic area could be the daily neuronal signal from the suprachiasmatic nucleus responsible for the timing of the luteinizing hormone surge. Vasopressin (50 ng/microl) or Ringer solution was administered by reverse microdialysis from Zeitgeber times 7.5 to 12.5 into the medial preoptic area of ovariectomized, estradiol-treated rats. The suprachiasmatic nucleus was lesioned to remove all cyclic luteinizing hormone secretion. This was evaluated by monitoring behavioral activity; animals that were arrhythmic were included in the experiments. Hourly blood samples were taken to measure plasma luteinizing hormone levels. Preoptic vasopressin administration induced a surge-like luteinizing hormone pattern in suprachiasmatic nucleus-lesioned animals, whereas constant, basal luteinizing hormone levels were found in the control animals. These data show that vasopressin, by itself, is able to trigger the luteinizing hormone surge in suprachiasmatic nucleus-lesioned rats. We propose that vasopressin is a timing signal from the suprachiasmatic nucleus responsible for the activation of the hypothalamo-pituitary-gonadal axis in the female rat.
雌性大鼠促黄体生成素激增是视前内侧区多种信号整合的结果。视前内侧区含有负责释放促黄体生成素的促性腺激素释放激素神经元、含有雌激素受体的神经元以及起源于视交叉上核的终末,例如以血管加压素作为神经递质。视前内侧区和视交叉上核对于促黄体生成素激增的发生都至关重要,因为损伤其中任何一个核都会阻止排卵前和类固醇诱导的促黄体生成素激增。在本研究中,我们调查了视前内侧区的血管加压素是否可能是来自视交叉上核的每日神经元信号,负责促黄体生成素激增的时间安排。通过反向微透析,在时间geber时间7.5至12.5将血管加压素(50纳克/微升)或林格氏液注入去卵巢、经雌二醇处理的大鼠的视前内侧区。对视交叉上核进行损伤以消除所有周期性促黄体生成素分泌。通过监测行为活动对此进行评估;无节律的动物被纳入实验。每小时采集血样以测量血浆促黄体生成素水平。在视交叉上核损伤的动物中,视前区给予血管加压素诱导出类似激增的促黄体生成素模式,而在对照动物中发现促黄体生成素水平持续处于基础状态。这些数据表明,血管加压素自身能够在视交叉上核损伤的大鼠中触发促黄体生成素激增。我们提出血管加压素是来自视交叉上核的时间信号,负责激活雌性大鼠的下丘脑 - 垂体 - 性腺轴。