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

雌激素和下丘脑细胞活性：发育效应和区域差异。

基本信息

批准号：
01480131
负责人：
SAKUMA Yasuo
金额：
$ 4.42万
依托单位：
Hirosaki University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (B)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1991
项目状态：
已结题

项目摘要

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

前凸反射是雌激素依赖性的雌性大鼠性行为的重要组成部分。我们研究了电刺激POA对自由活动、雌激素和孕酮治疗的卵巢切除大鼠脊柱前凸的影响，通过神经横断剥夺POA的隔传出，并与腹侧被盖区（VTA）的隔传出进行比较。切口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，但刺激横断的POA引起了对雄性坐骑的反应，其阈值为30 μ A，对脊柱前凸的迅速而强烈的抑制。最佳频率为50-100 Hz。当前应用终止后，脊柱前凸性能迅速恢复到刺激前水平。快速的时间过程将该效应与非去传入动物中的效应区分开来，后者发生缓慢且持续。在30 μ A和75-125 Hz下刺激VTA与刺激横突一样有效， ...更多信息截骨POA以快速和强烈抑制脊柱前凸。从POA或VTA阻断脊柱前凸时没有出现厌恶反应。电刺激这两个结构专门阻止脊柱前凸，而不破坏女性性行为的感受成分。因此，POA是脊柱前凸抑制机制中的一个独立和单独的实体。在683个POA神经元中，电刺激腹侧被盖区（VTA）可引起1.643.7ms的逆向激活，其中106只轻度乌拉坦麻醉大鼠的刺激阈值低至60 μ A。在记录前5-8天，在5-mm硅橡胶胶囊中给予雌激素，在每个动物组中比较雌激素的作用，该动物组包括38只作为成年切除卵巢的雌性大鼠（n=278，n，细胞数），38只雄性大鼠在出生当天去势（第1天，NC雄性）（n=181），和30只雌性大鼠（TP雌性）（n=224），在第5天给予1.25 mg睾酮，并作为成年大鼠切除卵巢。雌激素显著增加卵巢切除雌性（P<0.02，Mann-Whitney U检验）和NC雄性（P<0.04）的逆向激活阈值。前者不应期延长（P<0.02），逆行峰潜伏期延长（P<0.002）。在TP女性，没有参数受到雌激素的影响。因此，雌激素抑制了在发育过程中未暴露于睾酮的动物的POA轴突的兴奋性。（范围：2-40 ms）和刺激阈值（100-1，在10只正常大鼠中，电刺激中脑中央灰质后，测定了下丘脑腹内侧核（VMN）371个神经元（500 μ A（神经元数目，n=71）和29只切除睾丸的雄性大鼠，其接受无处理（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）。睾丸切除术显著降低逆向激活阈值。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。频率直方图的阈值表明，去氢睾酮达到这种效果，通过减少在低阈值范围内的细胞数量，而雌激素的作用是不对这部分细胞。睾酮给药动物的直方图与完整雄性动物的直方图相似。结果表明，不同的亚群的VMN神经元具有特定的敏感性睾酮的代谢产物项目的中央灰色，并可能支配不同方面的内分泌或情感controls.Long-term记录长达4天的自由移动的雌性大鼠在交配过程中遇到的男性微丝电极从POA的神经元。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）在显示脊柱前凸之前，神经元的活性短暂增加。少