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

前凸反射是雌性大鼠性行为中依赖雌激素的重要组成部分。我们研究了电刺激POA对自由运动、雌激素和黄体酮治疗的去卵巢大鼠前凸的影响，这些大鼠通过神经横断剥夺了POA的中隔传入神经，并与腹侧被盖区（VTA）的传入神经进行了比较。切口减少了引起最大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30muA阈值的男性坐骑的迅速而强烈的前凸抑制。最佳频率为50 ~ 100 Hz。在当前应用结束后，Lordosis的性能迅速恢复到开发前的水平。快速的时间过程将这种影响与未失足动物的影响区分开来，后者发生缓慢且持续。30muA和75 ~ 125 Hz的VTA刺激与transe刺激一样有效，更有效的POA引起快速而强烈的前凸抑制。POA或VTA的前凸阻断无不良反应。电刺激这两种结构都能阻断前凸，而不会破坏女性性行为的感知成分。因此，POA在前凸的抑制机制中是一个独立的实体。电刺激对失忆动物的放大效应可能是由于这种反射的促进电路被横断破坏。在683个POA神经元中，氨基乙酯麻醉大鼠的VTA刺激在1.643.7 ms的潜伏期内引起反激激活。106只大鼠轻度氨基甲酸乙酯麻醉刺激阈值低至60muA。在5毫米硅胶胶囊中记录前5-8天给予雌激素的影响，比较各组动物的效果，其中38只成年后切除卵巢的雌性大鼠（n=278, n，细胞数），38只出生当天阉割的雄性大鼠（n=181）， 30只成年后切除卵巢的雌性大鼠（TP雌性）（n=224）。雌激素显著提高了去卵巢女性（P<0.02， Mann-Whitney U检验）和正常卵巢男性（P<0.04）的逆行激活阈值。前者不应期延长（P<0.02），反峰潜伏期延长（P<0.002）。在TP雌性中，雌激素不影响任何参数。因此，雌性激素对发育过程中未暴露于雄性激素的动物的POA轴突的兴奋性有抑制作用。在氨基甲酸乙酯麻醉下，对10只完整雄性大鼠（神经元数量，n=71）和29只去兰雄性大鼠，分别给予未处理（10只，n=75）、丙酸睾酮（5只，n=75）、苯甲酸雌二醇（8只，n=77）和脱氢睾酮（6只，n=73），电刺激下丘脑腹内侧核（VMN） 371个神经元，测定了电刺激下丘脑腹内侧核（VMN） 371个神经元的反峰潜伏期（范围：2-40 ms）和刺激阈值（100- 1,500 mua）。兰花切除术显著降低了反激激活阈值。任何一种激素都能有效地将平均阈值提高到与完整雄性相当的值。阈值的频率直方图显示，脱氢睾酮通过在低阈值范围内减少细胞数量来达到这种效果，而雌激素对这部分细胞没有作用。注射睾酮的动物的直方图与未注射睾酮的雄性动物相似。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色，并可能控制内分泌或情感控制的不同方面。利用微丝电极对自由活动的雌性大鼠与雄性交配时的POA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)在前凸出现之前，神经元的活动会短暂增加。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