Different critical perinatal periods and hypothalamic sites of oestradiol action in the defeminisation of luteinising hormone surge and lordosis capacity in the rat.
Different critical perinatal periods and hypothalamic sites of oestradiol action in the defeminisation of luteinising hormone surge and lordosis capacity in the rat.
复制标题
雌二醇在大鼠黄体生成素激增和脊柱前凸能力去女性化中作用的不同关键围产期和下丘脑部位。
DOI：
10.1111/j.1365-2826.2012.02389.x
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发表时间：
2012
影响因子：
3.2
通讯作者：
榊原基嗣
中科院分区：
文献类型：
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作者：
Tomikawa J;Uenoyama Y;Ozawa M;Fukanuma T;Takase K;Goto T;Abe H;Ieda N;Minabe S;Deura C;Inoue N;Sanbo M;Tomita K;Hirabayashi M;Tanaka S;Imamura T;Okamura H;Maeda K-I;Tsukamura H.;榊原基嗣
雌性大鼠在排卵前雌激素水平下表现出促性腺激素释放激素（GnRH）/促黄体生成激素（LH）激增，而雄性大鼠则没有，因为在发育期间，围产期雌激素从雄激素转化为脑去雌性化。本研究旨在确定雌激素作用的部位和消除调节GnRH/LH峰机制的关键时期。检查了接受围产期治疗（如类固醇操作、雌二醇（E2）脑局部植入或NMDA拮抗剂给药）的动物在成年期显示E2诱导LH峰的能力。检查脊柱前凸行为，以比较GnRH/LH峰和性行为的去女性化机制。单次皮下在出生前一天（E21）、出生当天（D 0）或产后第5天（D5）给予苯甲酸雌二醇完全消除了雌性大鼠成年时E2诱导的LH峰，尽管相同的治疗没有抑制脊柱前凸。E21或D 0的围产期去势部分挽救了遗传雄性大鼠中E2诱导的LH峰，而E21至D5的去势完全挽救了脊柱前凸。在雌性大鼠中，下丘脑前部包括前腹侧室周核（AVPV）/视前区（POA）的E2植入消除了E2诱导的LH峰，而下丘脑中部和后部区域的E2植入对LH峰没有抑制作用。下丘脑任何区域的新生儿E2植入均不影响脊柱前凸。在雄性大鼠中，新生儿NMDA拮抗剂治疗挽救了脊柱前凸，但没有LH激增。综上所述，这些结果表明，下丘脑前区（如AVPV/POA区）是雌激素作用的围产期部位，在此GnRH/LH调节系统被去定位以消除雌激素诱导的激增。GnRH/LH峰系统的去女性化机制可能与性行为的机制不同，这与雌激素作用的部位和关键期以及所涉及的神经递质系统有关。
Female rats show a gonadotrophin‐releasing hormone (GnRH)/luteinising hormone (LH) surge in the presence of a preovulatory level of oestrogen, whereas males do not because of brain defeminisation during the developmental period by perinatal oestrogen converted from androgen. The present study aimed to identify the site(s) of oestrogen action and the critical period for defeminising the mechanism regulating the GnRH/LH surge. Animals given perinatal treatments, such as steroidal manipulations, brain local implantation of oestradiol (E2) or administration of an NMDA antagonist, were examined for their ability to show an E2‐induced LH surge at adulthood. Lordosis behaviour was examined to compare the mechanisms defeminising the GnRH/LH surge and sexual behaviour. A single s.c. oestradiol‐benzoate administration on either the day before birth (E21), the day of birth (D0) or day 5 (D5) postpartum completely abolished the E2‐induced LH surge at adulthood in female rats, although the same treatment did not inhibit lordosis. Perinatal castration on E21 or D0 partially rescued the E2‐induced LH surge in genetically male rats, whereas castration from E21 to D5 totally rescued lordosis. Neonatal E2implantation in the anterior hypothalamus including the anteroventral periventricular nucleus (AVPV)/preoptic area (POA) abolished the E2‐induced LH surge in female rats, whereas E2implantation in the mid and posterior hypothalamic regions had no inhibitory effect on the LH surge. Lordosis was not affected by neonatal E2implantation in any hypothalamic regions. In male rats, neonatal NMDA antagonist treatment rescued lordosis but not the LH surge. Taken together, these results suggest that an anterior hypothalamic region such as the AVPV/POA region is a perinatal site of oestrogen action where the GnRH/LH regulating system is defeminised to abolish the oestrogen‐induced surge. The mechanism for defeminisation of the GnRH/LH surge system might be different from that of sexual behaviour, in terms of the site(s) of oestrogen action and critical period, as well as the neurotransmitter system involved.