INTERACTION BETWEEN GLUTAMATE AND LUTEINIZING-HORMONE-RELEASING HORMONE (LHRH) IN LORDOSIS BEHAVIOR AND LUTEINIZING-HORMONE RELEASE (LH) - FURTHER-STUDIES ON NMDA RECEPTOR MEDIATION
INTERACTION BETWEEN GLUTAMATE AND LUTEINIZING-HORMONE-RELEASING HORMONE (LHRH) IN LORDOSIS BEHAVIOR AND LUTEINIZING-HORMONE RELEASE (LH) - FURTHER-STUDIES ON NMDA RECEPTOR MEDIATION
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DOI:
10.1016/0031-9384(95)00040-p
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发表时间:
1995-07-01
影响因子:
2.9
通讯作者:
DONOSO, AO
中科院分区:
文献类型:
--
作者:
GARGIULO, PA;DONOSO, AO
The present studies examine the effects of the glutamate agonist N-Methyl-D-Aspartic acid on lordosis responsiveness and LH release in estrogen-primed, ovariectomized rats. Groups of rats previously cannulated in the 3rd ventricle of the brain (IVT) were challenged with saline, NMDA and LHRH. A clear increase in lordosis-to-mount quotients (LQ) after 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 cases. Intraventricular administration of the selective LHRH antagonist [D-p-Glu(1), D-Phe(2), D-Trp(3,6)]-LHRH (100 ng) was unable to prevent NMDA action on lordosis behavior. In contrast, it blunted LHRH enhancement of LQ. LH release evoked by either NMDA and LHRH was blocked by the LHRH antagonist. Present results support our previous view suggesting that glutamate, through NMDA receptors, participates in the regulation of lordosis behavior. Glutamate seems to exert its actions in the behavioral and endocrine patterns through different mechanisms; the first seems not to be mediated by LHRH, but the endocrine effect operates via LHRH release.