NEUROENDOCRINE REGULATION OF AGGRESSIVE BEHAVIOR

睾丸激素（T）刺激 男性典型的攻击性行为的表现仍然存在争议。 这一问题的核心是必须界定 T的雄激素和雌激素代谢产物在促进 战斗行为。 为了解决这个基本问题， 激素在中枢神经系统中的作用，一种研究策略 它整合了对老鼠的行为和生化研究， 最近使用了许多不同的菌株。 基因型 不同的反应，以侵略促进 雄性小鼠具有雄激素和雌激素的特性 来自CF-1、CFW和CD-1菌株。 的这些差异 敏感性似乎与基因决定的 受体结合的差异。 更具体地说， 与雌激素（用己烯雌酚，DES测量）相关 结合位点的数目越多， DES-雌激素受体之间的结合。 DHT的结合， 在促进攻击性方面有中等效果的雄激素 在3个品系中， 方面的影响. 拟议的一系列实验的目标将是进一步 探索受体结合与行为之间的关系 通过使用综合的行为和 生化研究 这些研究将确定 K/d、B/max与对 DES的攻击促进属性可以扩展到其他 雌激素和雄激素或受体的其他方面 应检查结合（解离动力学、核结合） 来确定行为反应的分子关联 这些荷尔蒙。 此外，新生儿激素的作用 刺激是建立行为的生化基础， 在以后的生活中的反应也将被检查。 这些研究预计将支持一个假设， 受体结合和对药物的反应性之间的关系 雄激素和雌激素的侵略促进特性。 等 研究结果将大大提高我们对 参与激素调节的分子过程 小鼠的雄性间攻击行为，并可能促进 神经系统类固醇敏感性理论模型的建立 可以在未来的研究中评估的组织。

The mechanisms through which testosterone (T) stimulates the display of male-typical aggressive behavior remain controversial. At the center of this issue is the necessity for defining the role of the androgenic and estrogenic metabolites of T in the promotion of fighting behavior. To address this fundamental question about hormone action in the central nervous system, a research strategy that integrated behavioral and biochemical studies of mice from a number of different strains was recently employed. Genotypic differences in responsiveness to the aggression-promoting property of androgen and estrogen were found among male mice from the CF-1, CFW, and CD-1 strains. These differences in sensitivity appeared to be related to genetically determined differences in receptor binding. More specifically, responsiveness to estrogen (as measured with diethylstilbestrol, DES) was related to either a higher number of binding sites or higher affinity binding between DES-estrogen receptor. The binding of DHT, an androgen that was moderately effective in promoting aggression in the 3 strains, was not systematically related to its behavioral effects. The goal of the proposed series of experiments will be to further explore the relationship between receptor binding and behavioral responsiveness through the use of integrated behavioral and biochemical investigations. The studies will determine whether the relationship between K/d, B/max, and sensitivity to the aggression-promoting property of DES can be extended to other estrogens and androgens or whether additional aspects of receptor binding (dissociation kinetics, nuclear binding) should be examined to identify the molecular correlates of behavioral responsiveness to these hormones. In addition, the role of neonatal hormonal stimulation is establishing the biochemical basis for behavioral responsiveness later in life will also be examined. The studies are expected to support the hypothesis of a relationship between receptor binding and responsiveness to the aggression-promoting property of androgen and estrogen. Such findings would significantly enhance our understanding of the molecular processes involved in the hormonal regulation of intermale aggressive behavior in mice and may facilitate the development of a theoretical model of steroid sensitivity in neural tissues that can be assessed in future investigations.