Facilitation of estrous behavior by vaginal cervical stimulation in female rats involves alpha1-adrenergic receptor activation of the nitric oxide pathway.
In estrogen-primed female rats, vaginal cervical stimulation (VCS) provided by male intromissions or by an experimenter enhances estrous behaviors exhibited by females during subsequent mating with a male. We tested the hypothesis that alpha(1)-adrenergic receptors, acting via the nitric oxide-cGMP-protein kinase G pathway, mediate VCS-induced facilitation of female reproductive behaviors. Ovariectomized, estradiol-primed rats received intracerebroventricular (icv) infusions of vehicle or pharmacological antagonists 15 or 60min before VCS. Estrous behaviors (lordosis and proceptivity) in the presence of a male were recorded immediately (0min), and 120min following VCS. First we verified that VCS, but not manual flank stimulation alone, enhanced estrous behaviors when females received icv infusion of the vehicles used to administer drugs. Increased estrous behavior was apparent immediately following VCS and persisted for 120min. We then infused prazosin, phenoxybenzamine (alpha(1)-adrenergic receptor antagonists), yohimbine, idaxozan (alpha(2)-adrenergic receptor antagonists), or propranolol (beta-adrenergic receptor antagonist) 15min prior to the application of VCS in females primed with 5mug estradiol benzoate. Only alpha(1)-adrenergic antagonists inhibited VCS facilitation of estrous behavior, apparent 120min after VCS. Finally, we administered specific inhibitors of soluble guanylyl cyclase, nitric oxide synthase or protein kinase G icv 15 or 60min before VCS. All three agents significantly attenuated VCS facilitation of estrous behavior. These data support the hypothesis that endogenously released norepinephrine, acting via alpha(1)-adrenergic receptors, mediates the facilitation of lordosis by VCS, and are consistent with a mechanism involving alpha(1)-adrenergic activation of the nitric oxide/cGMP/protein kinase G pathway.
González-Flores
Oscar
O
Centro de Investigación en Reproducción Animal, Universidad Autónoma de Tlaxcala-CINVESTAV. Apdo. 62, Tlaxcala, Mexico. oglezflo@prodigy.net.mx
Beyer
Carlos
C
Lima-Hernández
Francisco Javier
FJ
Gómora-Arrati
Porfirio
P
Gómez-Camarillo
Madaí A
MA
Hoffman
Kurt
K
Etgen
Anne M
AM
D018663:Adrenergic Agents / Q000494:pharmacology; D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D003270:Contraceptive Agents / Q000494:pharmacology; D004347:Drug Interactions; D004791:Enzyme Inhibitors / Q000494:pharmacology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D030762:Estrous Cycle / Q000187:drug effects / Q000502:physiology*; D005260:Female; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism*; D010052:Ovariectomy / Q000379:methods; D010812:Physical Stimulation / Q000379:methods; D051381:Rats; D018340:Receptors, Adrenergic, alpha-1 / Q000502:physiology*; D012726:Sexual Behavior, Animal / Q000502:physiology*; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D014621:Vagina / Q000294:innervation*
D018663:Adrenergic Agents; D003270:Contraceptive Agents; D004791:Enzyme Inhibitors; D018340:Receptors, Adrenergic, alpha-1; C074283:estradiol 3-benzoate; D009569:Nitric Oxide; D004958:Estradiol