Department of Physiology, Center for Studies in Reproduction, School of Medicine, University of Maryland, Baltimore, Maryland 21201, USA.
J Neuroendocrinol. 1990 Apr 1;2(2):131-9. doi: 10.1111/j.1365-2826.1990.tb00842.x.
Abstract Recently, we reported that luteinizing hormone-releasing hormone (LHRH) neurons of estrogen-treated, ovariectomized rats have only limited responsiveness to norepinephrine (NE). These conclusions were based upon observations that NE, when infused intracerebroventricularly, produced only minor increases in plasma luteinizing hormone (LH), whereas, similar infusions following preliminary medial preoptic area (MPOA) electrochemical stimulation (ECS) markedly amplified LH secretion. One difficulty with this approach is that ECS produces an irritative lesion and deposits iron within the tissue, whereas, electrical stimulation (ES) does not have such effects. Accordingly, in the present study, we compared the effects of MPOA-ECS versus -ES on LHRH neuronal responsiveness to NE. While equivalent peak LH concentrations occurred within 15 min after MPOA-ECS or -ES, in the ECS group, LH release was sustained, whereas, it abruptly ceased upon termination of ES (at 15 min). The intracerebroventricular pulse infusion of NE at the time of peak LH secretion (30 min) in MPOA-ECS animals markedly amplified LH release. In these animals, plasma LH remained significantly elevated for 75 min before a decline was observed. In contrast, an infusion of NE at the time of maximal LH release in ES rats (16 min) did not augment LH secretion. The second series of studies examined the effects of MPOA infusions of NE in animals receiving preoptic ES. A single infusion of NE 16 min after ES (i.e. one min after termination of ES) did not amplify LH release, but when two NE pulses were given at 5 and 16 min after beginning preoptic ES, peak plasma LH levels were maintained for an additional 30 min before a decline occurred. Pretreatment of rats with a yS-adrenoreceptor antagonist (propranolol) or a monoamine oxidase inhibitor did not affect peak LH responses obtained after either MPOA-ES alone or combined with two pulses of NE infused into the MPOA at 5 and 16 min. We conclude that following cessation of MPOA-ES, LHRH neurons rapidly lose their responsiveness to NE, whereas, rats which received MPOA-ECS retain such responsiveness possibly due to the stimulative properties of the iron deposited by the ECS. Presumably, for NE to trigger an LH surge requires prior removal of some intrinsic inhibitory control which regulates LHRH neuronal responsiveness to NE.
摘要 最近，我们报道了雌激素处理的去卵巢大鼠的黄体生成素释放激素（LHRH）神经元对去甲肾上腺素（NE）的反应性有限。这些结论是基于以下观察结果：当 NE 经脑室输注时，仅轻微增加血浆黄体生成素（LH），而类似的输注在预先进行的中前脑区（MPOA）电化学刺激（ECS）后则显著放大 LH 分泌。这种方法的一个困难是，ECS 会产生刺激性损伤并在组织中沉积铁，而电刺激（ES）则没有这种作用。因此，在本研究中，我们比较了 MPOA-ECS 与 -ES 对 LHRH 神经元对 NE 的反应性的影响。虽然 MPOA-ECS 或 -ES 后 15 分钟内出现等效的 LH 峰值浓度，但在 ECS 组中，LH 释放持续，而 ES 终止时（15 分钟）则突然停止。在 MPOA-ECS 动物 LH 分泌峰值时，经脑室脉冲输注 NE 显著放大了 LH 释放。在这些动物中，血浆 LH 在观察到下降之前，在 75 分钟内仍保持显著升高。相比之下，在 ES 大鼠 LH 释放的最大时间（16 分钟）时输注 NE 并没有增强 LH 分泌。第二项研究检查了 MPOA 输注 NE 对接受视前 ES 动物的影响。在 ES 后 16 分钟（即 ES 终止后一分钟）单次输注 NE 并未放大 LH 释放，但当在视前 ES 开始后 5 分钟和 16 分钟时给予两次 NE 脉冲时，峰值血浆 LH 水平在下降之前再维持 30 分钟。用 yS-肾上腺素能受体拮抗剂（普萘洛尔）或单胺氧化酶抑制剂预处理大鼠，不会影响单独给予 MPOA-ES 或与在 5 分钟和 16 分钟时注入 MPOA 的两次 NE 脉冲联合给予时获得的 LH 峰值反应。我们得出结论，在 MPOA-ES 停止后，LHRH 神经元迅速失去对 NE 的反应性，而接受 MPOA-ECS 的大鼠则保持这种反应性，可能是由于 ECS 沉积的刺激特性所致。推测，NE 引发 LH 激增需要先去除调节 LHRH 神经元对 NE 反应性的某些内在抑制性控制。
