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

AuthorsCardona-Gómez, G. P.; Trejo, José L. ; Fernández García, Ana María ; García-Segura, Luis M.
Issue Date2000
PublisherLippincott Williams & Wilkins
CitationNeuroReport 11: 1735- 1738 (2000)
AbstractPrevious 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 estrogeninduced synaptic decrease. This finding suggest that estrogeninduced synaptic plasticity in the arcuate nucleus is dependent on the activation of both estrogen receptors and IGF-I receptors. (C) 2000 Lippincott Williams and Wilkins.
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