Gargiulo P A, Donoso A O
Laboratorio de Investigaciones Cerebrales (LINCE), Facultad de Ciencias Médicas, U.N.C., Mendoza, Argentina.
Physiol Behav. 1995 Jul;58(1):169-73. doi: 10.1016/0031-9384(95)00040-p.
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 microgram 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-Glu1, D-Phe2, D-Trp3,6]-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.
本研究检测了谷氨酸激动剂N-甲基-D-天冬氨酸对雌激素预处理的去卵巢大鼠脊柱前凸反应性和促黄体激素（LH）释放的影响。对先前已在脑第三脑室插管（脑室内插管）的大鼠组分别给予生理盐水、N-甲基-D-天冬氨酸（NMDA）和促黄体激素释放激素（LHRH）进行刺激。发现在脑室内给予0.5、0.75和1微克NMDA后，脊柱前凸与骑跨商数（LQ）明显增加。LHRH（150纳克，脑室内给药）也增强了LQ。在这两种情况下均出现高血浆LH水平。脑室内给予选择性LHRH拮抗剂[D-p-Glu1，D-Phe2，D-Trp3,6]-LHRH（100纳克）无法阻止NMDA对脊柱前凸行为的作用。相反，它减弱了LHRH对LQ的增强作用。LHRH拮抗剂阻断了由NMDA和LHRH诱发的LH释放。目前的结果支持我们之前的观点，即谷氨酸通过NMDA受体参与脊柱前凸行为的调节。谷氨酸似乎通过不同机制在行为和内分泌模式中发挥作用；第一种机制似乎不是由LHRH介导的，但内分泌效应是通过LHRH释放起作用的。
