Molecular mechanisms invovlved in sexual differentiation of the rat brain

脑侧脑室注射神经生长因子抗体阻断睾酮诱导的新生雌性大鼠行为去雌性化。在接受卵巢切除术和雌激素-孕激素联合治疗后的成年动物测试中，注射动物的前凸系数明显高于注射睾酮的正常兔兔血清对照组。阴道打开失败和阴蒂增大表明睾酮对实验动物和对照动物的生殖器有充分的男性化作用。在实验动物中，负责诱导前凸的下丘脑神经元的雌激素敏感性被保留。实验动物在刺激中脑中枢灰区后下丘脑腹内侧核神经元的逆行动作电位记录显示，雌激素降低了下丘脑逆行激活阈值，缩短了下丘脑传入神经的绝对不应期，同时也导致了雌激素诱导的行为激活。在对照组中，雌激素诱导的神经元激活与行为激活一起消失。

Injection of antibody to nerve growth factor into the cerebral lateral ventricle blocked testosterone-induced behavioral defeminization of neonatal female rat. When tested as adults following ovariectomy and the combined estrogen-progesterone treatment, the injected animals showed a significantly higher lordosis quotient than the testosterone-treated, normal rebbit serum infused controls. Failure of vaginal opening and clitoral enlargement manifested the well-documented masculinizing effect of testosterone on the genitalia in the experimental as well as the control animals. Estrogen-sensitivity of hypothalamic neurons which are responsible for the induction of lordosis was retained in the experimental animals. Recordings of the antidromic action potentials from neurons in the ventromedial nucleus of the hypothalamus following stimulation of the midbrain central gray revealed that estrogen decreased the antidromic activation threshold and shortened the absolute refractory period of th e hypothalamic efferents along with the estrogen-induced behavioral activation in the experimental animals. In the control group, the estrogen-induced neuronal activation was lost altogether with the behavioral activation.