Modulation of lordosis behavior by stimulation of noradrenergic receptor subtypes was examined in ovariectomized, estradiol benzoate (10 µg)-primed guinea pigs. In the first experiment, subcutaneous administration of the alpha-2-noradrenergic agonist, UK-14,304 (0.01, 0.5, or 1.0 mg/kg, Pfizer Central Research), produced a significant increase in lordosis behavior when these animals were compared with estrogen-primed control animals injected with saline. In a second experiment, estrogen-primed animals were injected with the alpha-1-noradrenergic agonist methoxamine (0.5 mg/ kg, s.c), UK-14,304 (0.5 mg/kg, s.c), or both drugs given together. Methoxamine or UK-14,304 administered alone facilitated lordosis in fewer than 50% of animals (17 and 39%, respectively). However, when both drugs were given together, 76% of the animals became sexually receptive. A third experiment showed that lordosis behavior facilitated by UK-14,304 could be attenuated by the administration of the alpha-2-noradrenergic antagonist idazoxan (2.5 mg/kg, s.c). Only 29% of sexually receptive animals (i.e. those animals primed with estradiol benzoate plus UK-14,304) continued to show lordosis after they received idazoxan. The results obtained from these and previously reported experiments suggest that both alpha-1- and alpha-2-noradrenergic receptors are involved in the regulation of lordosis behavior in the guinea pig.

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