INTERACTION BETWEEN GLUTAMATE AND LUTEINIZING-HORMONE-RELEASING HORMONE (LHRH) IN LORDOSIS BEHAVIOR AND LUTEINIZING-HORMONE RELEASE (LH) - FURTHER-STUDIES ON NMDA RECEPTOR MEDIATION

The present studies examine the effects of the glutamate agonist N-Met hyl-D-Aspartic acid on lordosis responsiveness and LH release in estro gen-primed, ovariectomized rats. Groups of rats previously cannulated in the 3rd ventricle of the brain (IVT) were challenged with saline, N MDA and LHRH. A clear increase in lordosis-to-mount quotients (LQ) aft er IVT administration of 0.5, 0.75 and 1 ug NMDA was found. LHRH (150 ng IVT) also enhanced LQ. High plasma LH levels were present in both c ases. Intraventricular administration of the selective LHRH antagonist [D-p-Glu(1), D-Phe(2), D-Trp(3,6)]-LHRH (100 ng) was unable to preven t NMDA action on lordosis behavior. In contrast, it blunted LHRH enhan cement of LQ. LH release evoked by either NMDA and LHRH was blocked by the LHRH antagonist. Present results support our previous view sugges ting that glutamate, through NMDA receptors, participates in the regul ation of lordosis behavior. Glutamate seems to exert its actions in th e behavioral and endocrine patterns through different mechanisms; the first seems not to be mediated by LHRH, but the endocrine effect opera tes via LHRH release.