EFFECTS OF LESIONS IN THE ORGANUM VASCULOSUM LAMINA TERMINALIS ON THE HYPOTHALAMIC DISTRIBUTION OF LUTEINIZING-HORMONE-RELEASING HORMONE AND GONADOTROPIN-SECRETION IN THE OVARIECTOMIZED RAT
EFFECTS OF LESIONS IN THE ORGANUM VASCULOSUM LAMINA TERMINALIS ON THE HYPOTHALAMIC DISTRIBUTION OF LUTEINIZING-HORMONE-RELEASING HORMONE AND GONADOTROPIN-SECRETION IN THE OVARIECTOMIZED RAT
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DOI：
10.1210/endo-105-4-939
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发表时间：
1979-01-01
期刊：
影响因子：
4.8
通讯作者：
MCCANN, SM
中科院分区：
文献类型：
--
作者：
SAMSON, WK;MCCANN, SM
在去势大鼠的终板血管器（OVLT）中产生射频损伤，以检查 OVLT 中 LHRH 与正中隆起（ME）中 LHRH 的关系以及 OVLT 在控制促性腺激素分泌中的可能作用。在第一个实验中，在病变产生后 1、3 和 7 天，通过 RIA（放射免疫测定）测量，OVLT 破坏显着降低了含有 OVLT 和 ME 的组织块中的 LHRH 含量，但没有改变垂体促性腺激素含量的血清 LH [促黄体激素] 和 FSH [促卵泡激素] 水平。在第二个实验中，OVLT损伤同样没有改变去卵巢大鼠的血清促性腺激素或雌激素的负反馈作用；然而，由于 OVLT 破坏，黄体酮引起的促性腺激素激增几乎消失。 OVLT 区域、ME 以及这两个结构之间的区域中 LHRH 含量降低。双侧内侧视前区病变也没有改变雌激素的负反馈效应，但与假手术和未手术对照中观察到的情况相比，显着降低了孕激素诱导的 LH 和 FSH 激增，尽管程度低于 OVLT 病变。内侧间隔损伤仅导致峰值略有减少。视前和间隔病变不会改变检查区域的组织 LHRH 含量。 OVLT 中含有 LHRH 的元素对于控制强直性促性腺激素分泌不是必需的，但在黄体酮诱导的 LH 和 FSH 激增中起着重要作用。 OVLT 的破坏导致 ME 中组织 LHRH 含量减少。整个间隔视前区显然存在弥漫的 LHRH 产生细胞群，OVLT 损伤不仅破坏含有 LHRH 的末端，而且破坏穿过 OVLT 区域前往 ME 的含有 LHRH 的轴突。这些结果与控制 LH 和 FSH 分泌的双调节中心的概念一致，并表明 LHRH 通过轴突转运传递至 ME。
Radiofrequency lesions were generated in the organum vasculosum lamina terminalis (OVLT) of ovariectomized rats to examine the relationship of LHRH in the OVLT to that in the median eminence (ME) and the possible role of the OVLT in the control of gonadotropin secretion. In the 1st experiment, OVLT destruction significantly decreased LHRH content, as measured by RIA [radioimmunoassay], in blocks of tissue containing the OVLT and the ME at 1, 3 and 7 days after production of lesions but did not alter serum LH [lutropin] and FSH [follitropin] levels of pituitary gonadotropin content. In the 2nd experiment, OVLT lesions similarly did not alter serum gonadotropins or the negative feedback effect of estrogen in the ovariectomized rats; however, the progesterone-induced gonadotropin surge was nearly abolished as a result of OVLT destruction. LHRH content was reduced in the region of the OVLT, in the ME and in a zone between these 2 structures. Bilateral medial preoptic area lesions also did not alter the negative feedback effect of estrogen but markedly reduced the progesterone-induced LH and FSH surges in comparison with those seen in sham-operated and unoperated controls, albeit to a lesser degree than OVLT lesions. Medial septal lesions resulted in only a slight reduction in the surge. Preoptic and septal lesions did not alter tissue LHRH content in the areas examined. The LHRH-containing elements in the OVLT are not essential for the control of tonic gonadotropin secretion but play an important role in the progesterone-induced LH and FSH surges. Destruction of the OVLT resulted in a decrease in tissue LHRH content in the ME. A diffuse population of LHRH-producing cells apparently exists throughout the septal-preoptic regions and OVLT lesions destroy not only LHRH-containing terminals but also LHRH-containing axons passing through the region of the OVLT en route to the ME. These results are consistent with the concept of dual regulatory centers for the control of LH and FSH secretion and suggest that LHRH is delivered to the ME by axonal transport.