Estrogen and Hypothalamic Cell Activity : Developmental Effects and Regional Differences.

前凸反射是雌性大鼠性行为中的一种雌激素依赖性的基本成分。在自由活动、雌激素和黄体酮处理的去卵巢大鼠中，我们观察了POA对前凸的电刺激作用。切割减少了产生最大前凸所需的雌激素量。尽管去除了隔膜抑制，刺激横断的POA引起了对30微安阈值的雄性坐骑前凸的迅速和强烈的抑制。最佳频率为50~100赫兹。在当前应用终止后，前凸性能立即恢复到刺激前水平。快速的时间进程将这种影响与非去传入动物区分开来，后者发生缓慢且持续。在30微安和75-125赫兹的VTA刺激与刺激横断…一样有效更多的POA会导致对前凸的快速而强烈的抑制。POA或VTA对前凸的阻断无不良反应。对这两个结构的电刺激特别阻止了前凸，而不破坏女性性行为的前向成分。因此，POA在抑制前凸的机制中是一个独立的独立实体。电刺激在去传入动物中的夸大效应可能是由于横断对这种反射的易化回路的破坏。在683个POA神经元中，刺激乌拉坦麻醉大鼠的VTA在1.643.7ms的潜伏期引起逆行激活。106只大鼠在浅乌拉坦麻醉下的刺激阈值低至60微安。每组动物包括成年雌性去卵巢大鼠38只(n=278，n，细胞数)，出生当天(NC雄性)去势雄性大鼠38只(n=181)，出生第5天给予1.25 mg睾酮的雌性大鼠30只(n=224)。雌激素显著提高去卵巢雌性(P&lt；0.02，Mann-Whitney U检验)和正常雄性(P&lt；0.04)的逆行激活阈值。前者表现为不应期延长(P&lt；0.02)和逆向峰电位潜伏期延长(P&lt；0.002)。在雌性TP中，雌激素不影响任何参数。在乌拉坦麻醉下，测定了电刺激大鼠中脑中央灰质后下丘脑腹内侧核(VMN)371个神经元的逆行峰潜伏期(范围：2-40ms)和刺激阈值(100-1,500muA)。29只去睾丸的雄性大鼠不接受治疗(10只，n=75)、丙酸睾丸酮(5只，n=75)、苯甲酸雌二醇组(8只，n=77)和去氢睾酮(6只，n=73)。摘除显著降低了逆行激活阈值。任何一种激素都有效地将平均阈值提高到与完整男性相当的值。阈值的频率直方图显示，脱氢睾酮通过减少低阈值范围内的细胞数量实现了这一效果，而雌激素对这部分细胞没有作用。接受睾丸激素处理的动物的直方图与完整雄性动物的直方图相似。结果表明，对睾酮代谢产物具有特殊敏感性的不同亚群的VMN神经元投射到中央灰质，并可能控制内分泌或情感控制的不同方面。在自由活动的雌性大鼠与雄性交配过程中，用微丝电极对POA神经元进行了长达4天的长期记录。我们发现(1)神经元对男性伴侣的阴道刺激有特异性反应，(2)那些在出现前凸之前活动短暂增加的神经元。较少

Lordosis reflex is an estrogen-dependent, essential component of the female rat sexual behavior. We examined electrical stimulation effects of the POA on lordosis in the free-moving, estrogen- and progesterone-treated ovariectomized 'rats, which were deprived of septal efferents of the POA by neural transections and compared with those of the ventral tegmental area (VTA). The cut reduced the amount of estrogen needed to elicit maximal lordosis. In spite of the removal of septal inhibition, stimulation of the transected POA caused a prompt and strong suppression of lordosis in response to male mounts with a threshold at 30muA. The optimal frequency was at 50-100 Hz. Lordosis performance returned promptly to the prestimulation level after the termination of current application. The rapid time course distinguished the effect from that in the non-deafferented animals, , which occurred slowly and persisted. VTA stimulation at 30muA and 75-125 Hz was as effective as stimulation of the transe … More cted POA to cause a rapid and strong suppression of lordosis. No aversive response accompanied the blockade of lordosis form the POA or VTA. Electrical stimulation of both structures specifically blocked lordosis, without disrupting the proceptive components of the female-sexual behavior. Thus, the POA is an independent and separate entity in the Inhibitory mechanism of lordosis. The exaggerated effect of electrical stimulation in the deafferented animals may result from a desruption of facilitative circuitry-for this reflex by the transection.In 683 POA neurons, VTA stimulation in urethane-anesthetized rats caused antidromic activation at latencies ranging 1.643.7 ms. Stimulus threshold was as low as 60muA in 106 rats under light urethane anaesthesia. Effects of estrogen, given 5-8 days prior to the recording in a 5-mm Silastic capsule, were compared within each animal group, which consisted of 38 female rats ovariectomized as adults (n=278, n, number of cells), 38 male rats castrated on the day of birth (day 1, NC males) (n=181), and 30 female rats given 1.25 mg testosterone on day 5 and ovariectomized as adults (TP females) (n=224). estrogen significantly increased the antidromic activation threshold in the ovariectomized females (P<0.02, Mann-Whitney U test) and in the NC males (P<0.04). In the former, the prolonged refractory period (P<0.02) and antidromic spike latency (P<0.002) were also detected. In the TP females, no parameter was affected by estrogen. Thus estrogen depressed the excitability of the POA axons in animals which had not been exposed to testosterone during the development.In animals under urethane anesthesia, antidromic spike latency (range : 2-40 ms) and stimulus threshold (100-1, 500muA) were determined for 371 neurons in the ventromedial hypothalamic nucleus (VMN) following electrical stimulation of the mid-brain central grey In 10 intact (number of neurons, n=71) and 29 orchidectomized male rats, which received either no treatment (10 rats, n=75), testosterone propionate (5 rats, n=75), estradiol benzoate (8 rats, n=77) or dehydrotestosterone (6 rats, n=73). Orchidectomy significantly decreased antidromic activation thresholds. Either hormone was effective to raise the mean threshold to values comparable to that in the intact males. Frequency histograms of the threshold showed that dehydrotestosterone achieved this effects by decreasing the number of cells at a low threshold range, whereas the action of estrogen was not on this fraction of cells. The histogram for the testosterone-treated animals was similar to that in the intact males. The results suggest that different subgroups of VMN neurons with specific sensitivity to metabolites of testosterone project to the central grey, and may govern different aspects of endocrine or affective controls.Long-term recordings up to 4 days were made from neurons in the POA in free-moving female rats during the copulatory encounter with males by microwire electrodes. We found (1) neurons specifically respond to vaginal stimulation by the male partner, and (2) those with a brief increase in their activity prior to the display of lordosis. Less