Kumar V, Lincoln G A, Tortonese D J
MRC Reproductive Biology Unit, Centre for Reproductive Biology, Edinburgh, Scotland, UK.
J Neuroendocrinol. 1993 Dec;5(6):649-54. doi: 10.1111/j.1365-2826.1993.tb00535.x.
To assess the role of excitatory amino acids (EAA) as neurotransmitters in the transmission of light information from the retina to the pineal gland, we have determined whether the systemic injection of EAA agonists in Soay rams will mimic the suppressive effect of light on the secretion of melatonin, and whether pretreatment of rams with EAA antagonists will block this effect. In addition, the efficacy of the drugs in affecting neuroendocrine systems was investigated by measuring the changes in the secretion of luteinizing hormone (LH) and prolactin. Injections fo the EAA receptor agonist, NMDA (N-methyl-D,L-aspartate: 4.0 mg/kg iv), and the non-NMDA type EAA receptor agonist, AMPA (DL-alpha-amino-3-hydroxy-5-methylisoxazole-propionic acid: 0.2 mg/kg iv) given at night to rams exposed to long days (16 h light: 8 h darkness), caused no change in the blood plasma concentrations of melatonin. The treatments induced an acute increase in the concentrations of LH, and NMDA, but not AMPA, caused a sustained increase in the concentrations of prolactin. Injections of the specific NMDA-type receptor antagonist, CGP (CGP 37849: 1.0 mg/kg iv) and the non-NMDA-type receptor antagonist, DNQX (6,7 Dinitroquinoxaline-2,3-dione: 0.5 mg/kg iv), given prior to a 1-h light period at night, in rams under long days, caused no change in the light-induced decrease in blood plasma concentrations of melatonin. The drug treatments had no effect on the plasma concentrations of LH, but CGP, and not DNQX, stimulated an acute increase in the plasma concentrations of prolactin. These results provide support for the hypothesis that EAA mechanisms operate in the hypothalamus to regulate the release of peptides and catecholamines which control the secretion of LH and prolactin from the pituitary gland; different sub-types of EAA receptors are involved in the control of the two pituitary hormones. The failure of the treatments to affect the secretion of melatonin may indicate that EAA receptor activation is not involved in the photic relay to the pineal gland, or may merely reflect the inability of the drugs to penetrate into the retina/SCN/pineal neural circuits to produce a response.
为了评估兴奋性氨基酸（EAA）作为神经递质在光信息从视网膜向松果体传递过程中的作用，我们确定了向索艾公羊全身注射EAA激动剂是否会模拟光对褪黑素分泌的抑制作用，以及用EAA拮抗剂预处理公羊是否会阻断这种作用。此外，通过测量促黄体生成素（LH）和催乳素分泌的变化，研究了这些药物对神经内分泌系统的影响。在长夜（16小时光照：8小时黑暗）条件下，于夜间给公羊静脉注射EAA受体激动剂N-甲基-D，L-天冬氨酸（NMDA：4.0毫克/千克）和非NMDA型EAA受体激动剂α-氨基-3-羟基-5-甲基异恶唑-4-丙酸（AMPA：0.2毫克/千克），血浆褪黑素浓度未发生变化。这些处理导致LH浓度急性升高，NMDA而非AMPA使催乳素浓度持续升高。在长夜条件下，于夜间1小时光照期之前给公羊静脉注射特异性NMDA型受体拮抗剂CGP（CGP 37849：1.0毫克/千克）和非NMDA型受体拮抗剂6,7-二硝基喹喔啉-2,3-二酮（DNQX：0.5毫克/千克），光照诱导的血浆褪黑素浓度降低未发生变化。药物处理对LH的血浆浓度没有影响，但CGP而非DNQX刺激催乳素血浆浓度急性升高。这些结果支持了以下假说：EAA机制在下丘脑中发挥作用，调节肽类和儿茶酚胺的释放，而这些肽类和儿茶酚胺控制着垂体中LH和催乳素的分泌；不同亚型的EAA受体参与了对这两种垂体激素的调控。处理未能影响褪黑素的分泌，这可能表明EAA受体激活不参与向松果体的光信号传递，或者可能仅仅反映出药物无法穿透视网膜/视交叉上核/松果体神经回路以产生反应。
