Evidence for the involvement of central 5-HT1A receptors in the mediation of lordosis behavior in the female rat.

5-Hydroxy-L-tryptophan (5-HTP), 25 mg kg-1 IP, in combination with the peripheral 5-HTP decarboxylase inhibitor benserazide, 25 mg kg-1 IP, and the selective inhibitor of neuronal 5-hydroxytryptamine (5-HT) re-uptake, zimeldine, 10 mg kg-1 IP, suppressed lordosis in ovariectomized female rats, treated with estradiol benzoate (EB) or with EB plus progesterone (P). The suppression of lordosis produced by 5-HTP was antagonized by the beta-receptor blocker (-)pindolol, which also is a selective 5-HT1 receptor antagonist, but not by the 5-HT2 receptor antagonists metitepine or pirenperone, nor by the beta-receptor blocker betaxolol. The EB- or EB plus P-activated lordosis was also suppressed by administration of the selective 5-HT1A receptor agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT). Together, these observations indicate an important role of central 5-HT1A receptors in the mediation of lordosis behavior in the female rat.