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N-甲基-D-天冬氨酸受体通过视网膜下丘脑束参与光信息的神经元传递。

N-methyl-D-aspartate receptor participates in neuronal transmission of photic information through the retinohypothalamic tract.

作者信息

Ohi K, Takashima M, Nishikawa T, Takahashi K

机构信息

Division of Mental Disorder Research, National Institute of Neuroscience, Tokyo, Japan.

出版信息

Neuroendocrinology. 1991 Apr;53(4):344-8. doi: 10.1159/000125740.

DOI:10.1159/000125740
PMID:1675438
Abstract

In order to assess the hypothesis that excitatory amino acids (EAA) are involved in the transmission of light information from retina to suprachiasmatic nucleus (SCN) and pineal via the retinohypothalamic tract (RHT), we have determined whether injections of EAA agonist into SCN could mimic the suppressive effects of light pulse on pineal melatonin production, and whether pretreatment with antagonists could block effects of light pulse in the intact rat. Injection of the EAA agonist N-methyl-D-aspartate (NMDA: 1.0 mM; 0.5 microliter) into the SCN suppressed plasma melatonin level and pineal N-acetyltransferase activity. The pretreatment with D-aminophosphonovalerate (D-APV: 2.5 or 10 mM; 2.0 microliters) or N-[1-(2-thienyl)-cyclohexyl]-piperidine (10 mM; 2.0 microliters) which are NMDA type receptor antagonists blocked the suppressive effect of the light pulse (3.0 Ix for 2 min), while the pretreatment with neither vehicle nor L-APV (optic isomer APV: 10 mM; 2.0 microliters) could block the effect of light. Alpha-D-glutamyl-amino-methylsulfonate (10 mM; 2.0 microliters or 25 mM; 2.0 microliters), which is a relative antagonist for non-NMDA type receptor, had no effect, either. These results suggest that EAA is involved in the transmission of light information through RHT and that in rat SCN EAA operates at the NMDA type receptor on the SCN.

摘要

为了评估兴奋性氨基酸(EAA)通过视网膜下丘脑束(RHT)参与光信息从视网膜到视交叉上核(SCN)和松果体传递的假说,我们已确定向SCN注射EAA激动剂是否能模拟光脉冲对松果体褪黑激素分泌的抑制作用,以及用拮抗剂预处理是否能在完整大鼠中阻断光脉冲的作用。向SCN注射EAA激动剂N-甲基-D-天冬氨酸(NMDA:1.0 mM;0.5微升)可抑制血浆褪黑激素水平和松果体N-乙酰转移酶活性。用NMDA型受体拮抗剂D-氨基磷酸戊酸(D-APV:2.5或10 mM;2.0微升)或N-[1-(2-噻吩基)-环己基]-哌啶(10 mM;2.0微升)预处理可阻断光脉冲(3.0勒克斯,持续2分钟)的抑制作用,而用溶剂或L-APV(光学异构体APV:10 mM;2.0微升)预处理均不能阻断光的作用。非NMDA型受体的相对拮抗剂α-D-谷氨酰-氨基甲基磺酸盐(10 mM;2.0微升或25 mM;2.0微升)也无作用。这些结果表明,EAA参与通过RHT的光信息传递,并且在大鼠SCN中,EAA作用于SCN上的NMDA型受体。

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