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Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York 10461
Address all correspondence and requests for reprints to: Dr. Anne M. Etgen, Department of Neuroscience, F113, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New York 10461. E-mail: etgen{at}aecom.yu.edu.
Estradiol (E2) regulates female reproductive behavior (lordosis) by acting on estrogen-sensitive neurons. We recently showed that E2 facilitation of lordosis behavior requires concurrent activation of brain IGF-I receptors. The present study confirmed this finding and sought to identify the downstream signaling pathways involved in estrogen/IGF-I priming of lordosis. Intracerebroventricular infusions of a selective IGF-I receptor antagonist were administered to ovariectomized rats every 12 h beginning 1 h before the first of two daily E2 injections. IGF-I receptor blockade partially inhibits lordosis if the antagonist is infused throughout the 2-d estrogen treatment period but not if it is administered only during the first or last 12 h of estrogen treatment. Because E2 and IGF-I can activate phosphatidylinositol-3-kinase (PI3K) and MAPK, we infused agents that block PI3K and/or MAPK activity as described above. Both PI3K inhibitors (wortmannin and LY294002) and MAPK inhibitors (PD98059 and U0126) partially attenuate lordosis when administered during estrogen priming. None of these drugs modifies lordosis if they are infused only once, during the last 12 h of estrogen treatment. When both wortmannin and PD98059 are infused during E2 priming, lordosis behavior is completely abolished. These data suggest that activation of both PI3K and MAPK by E2 and IGF-I mediates hormonal facilitation of lordosis behavior.
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O. Gonzalez-Flores, J. Shu, I. Camacho-Arroyo, and A. M. Etgen Regulation of Lordosis by Cyclic 3',5'-Guanosine Monophosphate, Progesterone, and Its 5{alpha}-Reduced Metabolites Involves Mitogen-Activated Protein Kinase Endocrinology, December 1, 2004; 145(12): 5560 - 5567. [Abstract] [Full Text] [PDF]
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