Estrogen receptors and insulin-like growth factor-I receptors mediate estrogen-dependent synaptic plasticity.
Neuroreport
; 11(8): 1735-8, 2000 Jun 05.
Article
em En
| MEDLINE
| ID: mdl-10852234
ABSTRACT
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Sinapses
/
Fator de Crescimento Insulin-Like I
/
Receptores de Estrogênio
/
Receptores de Somatomedina
/
Estradiol
/
Estrogênios
/
Plasticidade Neuronal
Limite:
Animals
Idioma:
En
Ano de publicação:
2000
Tipo de documento:
Article