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

脊柱前凸反射是雌性大鼠性行为的重要组成部分，依赖于雌激素。我们检查了 POA 对自由活动的雌激素和黄体酮治疗的切除卵巢大鼠的脊柱前凸的影响，这些大鼠通过神经横断剥夺了 POA 的间隔传出神经，并与腹侧被盖区 (VTA) 的间隔传出神经进行了比较。削减减少了引起最大脊柱前凸所需的雌激素量。尽管去除了间隔抑制，但对横断的 POA 的刺激引起了对雄性坐骑的迅速而强烈的脊柱前凸抑制，阈值为 30muA。最佳频率为 50-100 Hz。当前应用终止后，脊柱前凸表现立即恢复至刺激前水平。快速的时间过程将这种效应与非耳聋动物的效应区分开来，后者发生缓慢且持续。 30μA 和 75-125 Hz 的 VTA 刺激与刺激跨侧 POA 一样有效，可以快速而强烈地抑制脊柱前凸。 POA 或 VTA 的脊柱前凸受阻并无厌恶反应。对这两种结构的电刺激专门阻止了脊柱前凸，而不会破坏女性性行为的感知成分。因此，POA 在脊柱前凸的抑制机制中是一个独立且独立的实体。电刺激对传入神经迟钝的动物的夸大效果可能是由于横断造成的这种反射的促进电路的破坏所致。在 683 个 POA 神经元中，乌拉坦麻醉的大鼠中的 VTA 刺激引起潜伏期为 1.643.7 ms 的逆向激活。 106 只大鼠在轻度聚氨酯麻醉下的刺激阈值低至 60μA。记录前 5-8 天在 5 毫米硅橡胶胶囊中给予雌激素的影响，在每个动物组内进行比较，该动物组包括 38 只成年雌性大鼠（n=278，n，细胞数）、38 只在出生当天阉割的雄性大鼠（第 1 天，NC 雄性）（n=181），以及 30 只雌性大鼠在第 5 天和第 5 天给予 1.25 mg 睾酮。成年时切除卵巢（TP 女性）（n=224）。雌激素显着增加了切除卵巢的女性（P<0.02，Mann-Whitney U 检验）和 NC 男性（P<0.04）的逆向激活阈值。前者还检测到不应期延长（P<0.02）和逆向尖峰潜伏期（P<0.002）。在 TP 雌性中，没有参数受到雌激素的影响。因此，在发育过程中未接触过睾酮的动物中，雌激素会抑制 POA 轴突的兴奋性。 在乌拉坦麻醉下的动物中，在电刺激中脑中央灰质后，确定了下丘脑腹内侧核 (VMN) 中 371 个神经元的逆向尖峰潜伏期（范围：2-40 ms）和刺激阈值（100-1, 500muA）。 （神经元数量，n = 71）和 29 只睾丸切除的雄性大鼠，未接受治疗（10 只大鼠，n = 75）、丙酸睾酮（5 只大鼠，n = 75）、苯甲酸雌二醇（8 只大鼠，n = 77）或脱氢睾酮（6 只大鼠，n = 73）。睾丸切除术显着降低了逆向激活阈值。这两种激素都可以有效地将平均阈值提高到与完整雄性的水平相当的值。阈值的频率直方图表明，脱氢睾酮通过减少低阈值范围内的细胞数量来实现这种效果，而雌激素对这部分细胞没有作用。睾酮治疗动物的直方图与未受损伤的雄性动物的直方图相似。结果表明，对睾酮代谢物具有特定敏感性的VMN神经元的不同亚群投射到中央灰质，并且可能控制内分泌或情感控制的不同方面。在与雄性交配期间，通过微线电极对自由活动的雌性大鼠的POA中的神经元进行长达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）那些在表现出脊柱前凸之前其活动短暂增加的神经元。较少的

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