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 Previous Article
The Journal of Neuroscience, March 15, 2002, 22(6):2401-2408
Functional Interactions between Estrogen and Insulin-Like Growth
Factor-I in the Regulation of  1B-Adrenoceptors and
Female Reproductive Function
Arnulfo
Quesada and
Anne M.
Etgen
Department of Neuroscience, Albert Einstein College of Medicine,
Bronx, New York 10461
The ovarian hormone estradiol (E2) and
insulin-like growth factor-I (IGF-I) interact in the CNS to regulate
neuroendocrine function and synaptic remodeling. Previously, our
laboratory showed that 2 d E2 treatment induces
 1B-adrenoceptor expression and promotes IGF-I
enhancement of 1-adrenoceptor potentiation of cAMP
accumulation in the preoptic area (POA) and hypothalamus (HYP). This
study examined the hypothesis that E2-dependent aspects of
female reproductive function, including 1B-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 in vivo with vehicle or E2 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 E2 injection.
Administration of JB-1 during E2 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 1-adrenergic facilitation
of lordosis. In addition, blockade of IGF-IRs during E2
priming prevents E2-induced increases in
1B-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 E2 treatment. These events may help
coordinate the timing of ovulation with the expression of sexual receptivity.
Key words:
estradiol; IGF-I; adrenoceptor; hypothalamus; preoptic
area; reproduction
Copyright © 2002 Society for Neuroscience 0270-6474/02/2262401-08$05.00/0
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