Wayman C P, Wilson J F
Department of Pharmacology and Therapeutics, University of Wales College of Medicine, Heath Park, Cardiff, UK.
Neuroreport. 1991 Aug;2(8):481-4. doi: 10.1097/00001756-199108000-00018.
N-methyl-D-aspartic acid (NMDA) 10(-4) M stimulated release of immunoreactive alpha-melanocyte-stimulating hormone (alpha-MSH) from superfused slices of rat hypothalamus through receptors which shared common features with other central NMDA-type glutamate receptors. The receptors possessed inhibitory sites for both Mg2+ and ketamine; basal and NMDA-stimulated alpha-MSH release was reduced by high (5 mM) Mg2+ ion concentrations and by 10(-4) M ketamine, whilst use of Mg(2+)-free media led to a prolongation of the NMDA-stimulated response. The receptors were also shown to possess an allosteric glycine site. The glycine site agonist D-serine 10(-4) M potentiated basal and NMDA-stimulated alpha-MSH release whilst the antagonist, 7-chlorokynurenic acid 10(-4) M, reduced NMDA-stimulated release, an effect which was partially reversed by 10(-4) M D-serine.
N-甲基-D-天冬氨酸（NMDA）10⁻⁴ M通过与其他中枢NMDA型谷氨酸受体具有共同特征的受体，刺激大鼠下丘脑灌流切片释放免疫反应性α-黑素细胞刺激素（α-MSH）。这些受体对Mg²⁺和氯胺酮均具有抑制位点；高浓度（5 mM）的Mg²⁺离子和10⁻⁴ M氯胺酮可降低基础和NMDA刺激的α-MSH释放，而使用无Mg²⁺培养基会导致NMDA刺激反应的延长。这些受体还显示具有变构甘氨酸位点。甘氨酸位点激动剂D-丝氨酸10⁻⁴ M增强基础和NMDA刺激的α-MSH释放，而拮抗剂7-氯犬尿氨酸10⁻⁴ M降低NMDA刺激的释放，10⁻⁴ M D-丝氨酸可部分逆转该效应。
