Molecular mechanisms invovlved in sexual differentiation of the rat brain

侧脑室注射神经生长因子抗体可阻断睾酮诱导的新生雌性大鼠的行为脱髓。当成年后接受卵巢切除和雌激素-孕激素联合治疗的动物进行测试时，注射的动物显示出明显高于注射睾丸激素的正常反弹血清对照组的前凸商数。阴道开放和阴蒂扩大的失败表明，在实验动物和对照动物中，睾酮对生殖器的男性化作用是有据可查的。在实验动物中，负责诱导前凸的下丘脑神经元对雌激素的敏感性保持不变。刺激中脑中央灰质后记录的下丘脑腹内侧核神经元的逆行动作电位显示，雌激素使实验动物下丘脑传出神经元的逆行激活阈值降低，绝对不应期缩短，并伴随着雌激素诱导的行为激活。在对照组，雌激素诱导的神经元激活与行为激活完全消失。

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.