Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
8351689 | Pharmacology Biochemistry and Behavior | 2013 | 6 Pages |
Abstract
The present study tested the hypothesis that the Janus kinase 2, Src tyrosine kinases, and mitogen-activated protein kinase interact to regulate lordosis behavior induced by leptin in ovariectomized, estrogen-primed rats. The role of protein kinase A and protein kinase C in lordosis facilitation by leptin was also assessed. In experiment 1, the intracerebroventricular administration of leptin to ovariectomized, estradiol-primed rats significantly stimulated lordosis behavior at 1, 2 and 4Â h post-injection tests. In experiment 2, the Janus kinase 2 inhibitor AG490, the Src tyrosine kinase inhibitor PP2 and the mitogen-activated protein kinase inhibitor PD98059 were administered into the right lateral ventricle before leptin. The lordosis quotient and the lordosis score induced by leptin were significantly decreased by each of these kinase inhibitors. In experiment 3, we examined the effects of RpcAMPS and bisindolylmaleimide, protein kinase A and protein kinase C inhibitors on the lordosis elicited by leptin administration. Lordosis behavior induced by leptin was significantly decreased by both the protein kinase A and protein kinase C inhibitors at 1Â h post-leptin injection. The results confirm that multiple intracellular pathways participate in the expression of lordosis behavior in estrogen-primed rats elicited by leptin.
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Authors
Marcos GarcÃa-Juárez, Carlos Beyer, Porfirio Gómora-Arrati, Raymundo DomÃnguez-Ordoñez, Francisco J. Lima-Hernández, José R. Eguibar, Yadira L. Galicia-Aguas, Anne M. Etgen, Oscar González-Flores,