Kato M, Suzuki M, Kakegawa T
Endocrinology. 1985 Jan;116(1):382-8. doi: 10.1210/endo-116-1-382.
The object of the present experiments was to clarify the topography of hypothalamic areas related to the suppression of GH release induced by human pancreatic GH-releasing factor (hpGRF). One week before the experiments, bipolar concentric stimulating electrodes were implanted in the organum vasculosum of the lamina terminalis (OVLT), the periventricular nucleus of the hypothalamus (Pe), the ventromedial nucleus of the hypothalamus (VMH), the lateral hypothalamic area (LHA), or the ventral premammillary nucleus (PMV). At the same time, the jugular vein was cannulated for blood sampling, and lesion of the anterior Pe was performed with a cathodal current. One and one half hours before the first blood sampling the rats were anesthetized with pentobarbital to prevent spontaneous GH bursts. One minute after the first blood sampling, 10 micrograms hpGRF dissolved in 0.3 ml saline was injected iv through the cannula. The blood samples were collected at 10, 20, 30, and 60 min after the zero-time sample. The above mentioned hypothalamic nuclei were electrically stimulated for the first 10 min. Injection of hpGRF increased the plasma GH level from 44.2 +/- 7.3 ng/ml (mean +/- SE) to 981.4 +/- 59.8 ng/ml in 10 min, and the plasma GH level gradually decreased to 50.8 +/- 8.8 ng/ml by 60 min. The hpGRF-induced GH release was most effectively suppressed by the stimulation of the Pe. After the stimulation of the OVLT, the VMH, the LHA, or the PMV, the suppression of hpGRF-induced GH release was weaker than that of the Pe. This stimulation-induced suppression was fully or partly prevented in Pe-lesioned animals. These results indicate that the stimulation of the Pe, the OVLT, the VMH, the LHA, or the PMV exerts an inhibitory effect on GH release. For this inhibitory effect, the Pe was essential. The results are discussed with regard to the topography of immunoreactive SRIF neuronal cell bodies and processes in the hypothalamus.
本实验的目的是阐明与人类胰腺生长激素释放因子（hpGRF）诱导的生长激素（GH）释放抑制相关的下丘脑区域的局部解剖结构。实验前一周，将双极同心刺激电极植入终板血管器（OVLT）、下丘脑室周核（Pe）、下丘脑腹内侧核（VMH）、下丘脑外侧区（LHA）或腹侧乳头前核（PMV）。同时，对颈静脉进行插管用于采血，并用阴极电流对前Pe进行损伤。在第一次采血前1.5小时，用戊巴比妥麻醉大鼠以防止自发的GH脉冲。第一次采血后1分钟，将溶解于0.3 ml盐水中的10微克hpGRF通过插管静脉注射。在零时样品后的10、20、30和60分钟采集血样。上述下丘脑核在最初的10分钟内进行电刺激。注射hpGRF使血浆GH水平在10分钟内从44.2±7.3 ng/ml（平均值±标准误）升高至981.4±59.8 ng/ml，到60分钟时血浆GH水平逐渐降至50.8±8.8 ng/ml。刺激Pe能最有效地抑制hpGRF诱导的GH释放。刺激OVLT、VMH、LHA或PMV后，对hpGRF诱导的GH释放的抑制作用比刺激Pe时弱。在Pe损伤的动物中，这种刺激诱导的抑制作用被完全或部分阻止。这些结果表明，刺激Pe、OVLT、VMH、LHA或PMV对GH释放有抑制作用。对于这种抑制作用，Pe是必不可少的。结合下丘脑免疫反应性生长抑素释放因子（SRIF）神经元细胞体和突起的局部解剖结构对结果进行了讨论。
