Cardona-Gómez G P, Trejo J L, Fernandez A M, Garcia-Segura L M
Instituto Cajal, CSIC, Madrid, Spain.
Neuroreport. 2000 Jun 5;11(8):1735-8. doi: 10.1097/00001756-200006050-00027.
Previous studies have shown that estradiol induces a transient disconnection of axo-somatic inhibitory synapses in the hypothalamic arcuate nucleus of adult ovariectomized rats. The synaptic disconnection is accompanied by an increase in the levels of insulin-like growth factor-I (IGF-I) in the arcuate nucleus, suggesting that IGF-I signaling may be involved in the estrogen-induced synaptic plasticity. The role of estrogen receptors and IGF-I receptors in the synaptic changes has been studied by assessing the number of axo-somatic synapses in ovariectomized rats treated with intracerebroventricular administration of the estrogen receptor antagonist ICI 182,780 and the IGF-I receptor antagonist JBI to ovariectomized rats. Estradiol administration resulted in a significant decrease in the number of axo-somatic synapses on arcuate neurons in control ovariectomized rats. Both the estrogen receptor antagonist and the IGF-I receptor antagonist blocked the estrogen-induced synaptic decrease. This finding suggest that estrogen-induced synaptic plasticity in the arcuate nucleus is dependent on the activation of both estrogen receptors and IGF-I receptors.
先前的研究表明，雌二醇会导致成年去卵巢大鼠下丘脑弓状核中轴突-胞体抑制性突触出现短暂断开。这种突触断开伴随着弓状核中胰岛素样生长因子-I（IGF-I）水平的升高，这表明IGF-I信号传导可能参与了雌激素诱导的突触可塑性。通过评估向去卵巢大鼠脑室内注射雌激素受体拮抗剂ICI 182,780和IGF-I受体拮抗剂JBI的去卵巢大鼠中轴突-胞体突触的数量，研究了雌激素受体和IGF-I受体在突触变化中的作用。给予雌二醇导致对照去卵巢大鼠弓状神经元上的轴突-胞体突触数量显著减少。雌激素受体拮抗剂和IGF-I受体拮抗剂均阻断了雌激素诱导的突触减少。这一发现表明，弓状核中雌激素诱导的突触可塑性依赖于雌激素受体和IGF-I受体的激活。
