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875349 
Journal Article 
The nitric oxide pathway participates in lordosis behavior induced by central administration of leptin 
García-Juárez, M; Beyer, C; Gómora-Arrati, P; Lima-Hernández, FJ; Domínguez-Ordoñez, R; Eguibar, JR; Etgen, AM; González-Flores, O 
2012 
1 
Neuropeptides
ISSN: 0143-4179 
46 
1 
49-53 
English 
22019256 
WOS:000300268800006 
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) 30min before leptin administration (1μg). This dose of leptin reliably induced lordosis behavior in ovariectomized estradiol benzoate treated rats. The lordosis induced by leptin at 1 and 2h after infusion was significantly reduced by the previous injection of either L-NAME or by ODQ. Intracerebroventricular infusion of the PKG inhibitor (KT5823) 30min before leptin infusion, also significantly inhibited the lordosis behavior induced by leptin at 1 and 2h 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. 
Leptin; Lordosis behavior; Nitric oxide; Nitric oxide synthase; Cyclic GMP; L-NAME; ODQ; KT5823