Inhibition by N-methyl-D-aspartic acid (NMDA) receptor antagonist of lordosis behavior induced by estrogen followed by progesterone or luteinizing hormone-releasing hormone (LHRH) in the rat.

The effects of glutamate receptor antagonists on sexual receptivity induced by progesterone and LHRH were examined in ovariectomized, estradiol-primed rats (OVX-EB). Enhancement of lordosis/mounts quotient (L/M) by progesterone (0.5 mg) or LH-RH (150 ng; third ventricle, IVT) in OVX-EB rats was significantly decreased by IVT injection of (+) 2-amino-7-phosphonoheptanoic acid a competitive N-methyl-D-aspartic acid (NMDA) receptor antagonist. On the contrary, there were no changes in L/M quotient after IVT injection of 6,7-dinitroquinoxaline-2,3,dione at two dose levels, a Non-NMDA receptor antagonist. The NMDA antagonist did not modify lordosis behavior in OVX-EB rats. The results indicate that the NMDA type of glutamate receptors appears to mediate progesterone and LHRH facilitatory actions and suggest that glutamatergic synapses may be involved in lordosis-facilitating neural mechanisms.