The nitric oxide pathway participates in lordosis behavior induced by central administration of leptin

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• 作者：Marcos Garcí ; a-Juá ; rez^a ; ^b ; Carlos Beyer^a ; Porfirio Gó ; mora-Arrati^a ; Francisco J. Lima-Herná ; ndez^a ; Raymundo Domí ; nguez-Ordoñ ; ez^a ; José ; R. Eguibar^b ; Anne M. Etgen^c ; Oscar Gonzá ; lez-Flores^a ; ^{oglezflo@hotmail.com} ; ^{oglezflo@gmail.com}
• 关键词：Leptin ; Lordosis behavior ; Nitric oxide ; Nitric oxide synthase ; Cyclic GMP ; L-NAME ; ODQ ; KT5823
• 刊名：Neuropeptides
• 出版年：2012
• 出版时间：February 2012
• 年：2012
• 卷：46
• 期：1
• 页码：49-53
• 全文大小：268 K

文摘

Intracerebroventricular (icv) administration of leptin facilitates lordosis behavior in ad libitum-fed, estrogen-primed rats. The cellular mechanism involved in this response is unknown. The present study tested the hypothesis that the nitric oxide-guanylyl cyclase, cGMP-dependent protein kinase (PKG) pathway is involved in the facilitation of lordosis behavior induced by the central administration of leptin. We tested the importance of the nitric oxide/cGMP pathway for lordosis stimulation by either icv infusion of a nitric oxide synthase inhibitor (L-NAME) or a nitric oxide-dependent, soluble guanylyl cyclase inhibitor (ODQ) 30 min before leptin administration (1 ¦Ìg). This dose of leptin reliably induced lordosis behavior in ovariectomized estradiol benzoate treated rats. The lordosis induced by leptin at 1 and 2 h after infusion was significantly reduced by the previous injection of either L-NAME or by ODQ. Intracerebroventricular infusion of the PKG inhibitor (KT5823) 30 min before leptin infusion, also significantly inhibited the lordosis behavior induced by leptin at 1 and 2 h after hormone administration. These data support the hypothesis that the nitric oxide/cGMP/PKG pathway is involved in the facilitation of lordosis by leptin in estrogen-primed female rats.