Journal
NEUROREPORT
Volume 11, Issue 8, Pages 1735-1738Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/00001756-200006050-00027
Keywords
estradiol; estrogen receptors; insulin-like growth factor-I; synapses; synaptic plasticity
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Previous studies have shown that estradiol induces a transient disconnection 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 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 axe-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 axe-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. NeuroReport 11:1735-1738 (C) 2000 Lippincott Williams & Wilkins.
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