Estrogen receptors and insulin-like growth factor-I receptors mediate estrogen-dependent synaptic plasticity

Previous studies have shown that estradiol induces a transient disconnectio n of axe-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 arcu ate nucleus, suggesting that IGF-I signaling may be involved in the estroge n-induced synaptic plasticity. The role of estrogen receptors and IGF-I rec eptors in the synaptic changes has been studied by assessing the number of axe-somatic synapses in ovariectomized rats treated with intracerebroventri cular administration of the estrogen receptor antagonist ICI 182,780 and th e IGF-I receptor antagonist JBI to ovariectomized rats. Estradiol administr ation resulted in a significant decrease in the number of axe-somatic synap ses on arcuate neurons in control ovariectomized rats. Both the estrogen re ceptor antagonist and the IGF-I receptor antagonist blocked the estrogen-in duced synaptic decrease. This finding suggest that estrogen-induced synapti c plasticity in the arcuate nucleus is dependent on the activation of both estrogen receptors and IGF-I receptors. NeuroReport 11:1735-1738 (C) 2000 L ippincott Williams & Wilkins.