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Insulin-Like Growth Factor-1 Regulation of ₁-Adrenergic Receptor Signaling Is Estradiol Dependent in the Preoptic Area and Hypothalamus of Female Rats¹

Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461

Address all correspondence and requests for reprints to: Dr. Arnulfo Quesada, Department of Neuroscience, Albert Einstein College of Medicine, 1300 Morris Park Avenue, F113, Bronx, New York 10461. E-mail: quesada{at}aecom.yu.edu

Recently, we demonstrated that estradiol (E₂) modulates cross-talk between protein tyrosine kinases and norepinephrine (NE) receptor signaling in the hypothalamus (HYP) and preoptic area (POA), brain areas that govern female reproductive function. We are now investigating the identity of protein tyrosine kinase(s) that modify NE receptor signaling in the HYP and POA. Incubation of POA and HYP slices with insulin-like growth factor I (IGF-I), which signals via a receptor (IGF-IR) with endogenous tyrosine kinase activity, enhances NE-stimulated cAMP accumulation only in tissue derived from ovariectomized, E₂-primed animals. JB-1, an antagonist for IGF-IR, prevents the IGF-I enhancement of NE-stimulated cAMP accumulation in both POA and HYP slices. IGF-I enhances NE-stimulated cAMP accumulation via modulation of ₁-adrenoceptor potentiation of adenylyl cyclase. Binding studies in membranes demonstrate that ovariectomized, E₂-primed animals show a significant increase in the density of [¹²⁵I]IGF-I-binding sites in both POA and HYP compared with ovariectomized control animals. Neither the IC₅₀ for [¹²⁵I]IGF-I displacement by IGF-I nor the levels of IGF-I binding proteins in serum or brain tissue are affected by E₂. RIA results showed that E₂ does not modify serum or brain IGF-I levels. These results indicate that E₂ regulation of NE receptor function in the POA and HYP involves increased expression of IGF-IR, and that after E₂ treatment, IGF-IR activation augments ₁-adrenoceptor signaling.

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