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Based on pharmacological studies it has been suggested that the monoamines, and in particular serotonin and dopamine may inhibit female sexual behavior. Manipulations of other catecholamines and alterations in cholinergic systems may either facilitate or inhibit female sexual responses. A number of discrepancies exist in the literature and the present review hypothesizes that differential degrees of estrogen priming may explain some of the observed inter- and intraspecific differences. Additional possible mechanisms which may be related to drug induced facilitations of female sexual behavior are reviewed. It has been clearly demonstrated that adrenal secretions are not essential for drug induced increases in female sexual receptivity. It is possible that changes in hypothalamic luteinizing hormone-releasing hormone may underlie drug related changes in sexual receptivity. In addition data relevant to the possibility that drugs which facilitate lordosis may share a common mechanism of action with progesterone are examined. At present there is little direct support for either of the latter hypotheses. Drugs may also exert behavioral effects by changes in sensory or autonomic systems but pharmacological effects on these systems have not been adequately explored.