Sahu A, Kalra S P, Crowley W R, O'Donohue T L, Kalra P S
Endocrinology. 1987 May;120(5):1831-6. doi: 10.1210/endo-120-5-1831.
Intracerebroventricular administration of neuropeptide Y (NPY) has been shown to modify LH secretion, with the direction of the response dependent on the steroid background. To study further the role of gonadal steroids in the regulation of NPY secretion, the basal and KCl-evoked release of NPY from the medial basal hypothalamus (MBH) of intact and castrated male rats was assessed twice with the use of an in vitro incubation system. In each experiment, the amounts of NPY released in response to a 15-min pulse of KCl (45 mM) were significantly smaller from the MBH of castrated rats than of intact rats (P less than 0.05). Next, to assess the possible effects of prostaglandin E2 (PGE2), the MBH were exposed in a similar manner to two 15-min pulses, 30 min apart, of 0.568 and 56.8 mumol PGE2. Unlike KCl, PGE2 failed to stimulate NPY release from the MBH of either intact or castrated rats. However, a similar 56.8 mumol concentration of PGE2 was effective in stimulating the release of LHRH. We next examined the effects of castration on NPY levels in several microdissected regions of the hypothalamus. Whereas NPY concentrations were unchanged in the medial preoptic area, paraventricular nucleus and dorsomedial nucleus, NPY levels were significantly decreased in the median eminence, arcuate nucleus, and ventromedial nucleus 2 weeks after castration. These studies show that KCl can stimulate NPY release from the MBH in vitro, like that of LHRH, the KCl-induced NPY response is significantly smaller from the MBH of castrated than intact males, castration can significantly reduce the levels of NPY in the median eminence, arcuate nucleus, and ventromedial nucleus, thereby suggesting that testicular secretions may modulate NPY levels and release from the MBH, and because PGE2 stimulated the release of LHRH but not of NPY, separate regulatory neural events may underlie the secretion of these two neuropeptides.
脑室内注射神经肽Y（NPY）已被证明可改变促黄体生成素（LH）的分泌，其反应方向取决于类固醇背景。为了进一步研究性腺类固醇在调节NPY分泌中的作用，使用体外孵育系统对完整和去势雄性大鼠内侧基底下丘脑（MBH）中NPY的基础释放和氯化钾诱发的释放进行了两次评估。在每个实验中，去势大鼠MBH对15分钟氯化钾（45 mM）脉冲反应释放的NPY量明显少于完整大鼠（P<0.05）。接下来，为了评估前列腺素E2（PGE2）的可能作用，以类似方式将MBH暴露于间隔30分钟的两个15分钟脉冲的0.568和56.8 μmol PGE2中。与氯化钾不同，PGE2未能刺激完整或去势大鼠MBH释放NPY。然而，类似的56.8 μmol浓度的PGE2可有效刺激促性腺激素释放激素（LHRH）的释放。接下来，我们研究了去势对下丘脑几个显微切割区域中NPY水平的影响。虽然内侧视前区、室旁核和背内侧核中的NPY浓度未发生变化，但去势2周后，正中隆起、弓状核和腹内侧核中的NPY水平显著降低。这些研究表明，氯化钾在体外可刺激MBH释放NPY，与LHRH一样，去势雄性大鼠MBH对氯化钾诱导的NPY反应明显小于完整雄性大鼠，去势可显著降低正中隆起、弓状核和腹内侧核中的NPY水平，从而表明睾丸分泌物可能调节MBH中的NPY水平和释放，并且由于PGE2刺激了LHRH的释放而不是NPY的释放，这两种神经肽的分泌可能存在独立的调节神经事件。
