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Previously, our laboratory showed that 2 d E<jats:sub>2<\/jats:sub>treatment induces \u03b1<jats:sub>1B<\/jats:sub>-adrenoceptor expression and promotes IGF-I enhancement of \u03b1<jats:sub>1<\/jats:sub>-adrenoceptor potentiation of cAMP accumulation in the preoptic area (POA) and hypothalamus (HYP). This study examined the hypothesis that E<jats:sub>2<\/jats:sub>-dependent aspects of female reproductive function, including \u03b1<jats:sub>1B<\/jats:sub>-adrenoceptor expression and function in the POA and HYP, are mediated by brain IGF-I receptors (IGF-IRs) in female rats. Ovariohysterectomized rats were implanted with a guide cannula aimed at the third ventricle and treated<jats:italic>in vivo<\/jats:italic>with vehicle or E<jats:sub>2<\/jats:sub>daily for 2 d before experimentation. Intracerebroventricular infusions of JB-1, a selective IGF-IR antagonist, were administered every 12 hr beginning 1 hr before the first E<jats:sub>2<\/jats:sub>injection. Administration of JB-1 during E<jats:sub>2<\/jats:sub>priming completely blocks hormone-induced luteinizing hormone release and partially inhibits hormone-dependent reproductive behavior. Reproductive behavior is restored by intracerebroventricular infusion of 8-bromo-cGMP, the second messenger implicated in \u03b1<jats:sub>1<\/jats:sub>-adrenergic facilitation of lordosis. In addition, blockade of IGF-IRs during E<jats:sub>2<\/jats:sub>priming prevents E<jats:sub>2<\/jats:sub>-induced increases in \u03b1<jats:sub>1B<\/jats:sub>-adenoceptor binding density and abolishes acute IGF-I enhancement of NE-stimulated cAMP accumulation in HYP and POA slices. These data document the existence of a novel mechanism by which IGF-I participates in the remodeling of noradrenergic receptor signaling in the HYP and POA after E<jats:sub>2<\/jats:sub>treatment. 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