Drugs which alter nicotinic cholinergic transmission were administered to female rats to examine the neurochemical regulation of feminine sexual behavior. Nicotine (50, 100 or 200 micrograms/kg, IP) facilitated lordosis behavior 5 minutes after injection in estrogen-primed ovariectomized (OVX) rats. Pretreatment with the nicotinic antagonist, mecamylamine (MECA, 2.5 or 10 mg/kg) prevented this effect, while atropine pretreatment (30 mg/kg) reduced it. Mecamylamine pretreatment also reduced lordotic behavior induced by bilateral intracerebroventricular (ICV) injection of the cholinesterase inhibitor, eserine (5 micrograms/cannula). However, MECA treatment (5 or 10 micrograms/cannula, bilaterally, ICV, or 5 or 10 mg/kg, IP) did not reduce sexual receptivity in OVX rats made highly receptive with estrogen plus progesterone priming. By comparison with previously published results, MECA is apparently less effective than muscarinic antagonists in disrupting sexual receptivity in several paradigms. There appears to be a critical muscarinic link in the neural circuit for sexual receptivity, but there does not appear to be a comparable nicotinic link. In fact, the lordosis-facilitating effect of nicotine may be a pharmacological effect unrelated to the normal neurochemical regulation of sexual receptivity.