Paul K N, Fukuhara C, Tosini G, Albers H E
Center for Behavioral Neuroscience, Department of Biology, Georgia State University, 24 Peachtree Center Avenue, P.O. Box 4010, Atlanta, GA 30302-4010, USA.
Neuroscience. 2003;119(1):137-44. doi: 10.1016/s0306-4522(03)00098-8.
The suprachiasmatic nucleus (SCN) contains a circadian clock and regulates melatonin synthesis in the pineal gland. Light exposure during the subjective night acutely increases the mRNA levels of the Period (Per)1 gene in the SCN and acutely suppresses melatonin levels in the pineal gland. Activation of N-methyl-D-aspartate (NMDA) receptors in the SCN has been demonstrated to phase-shift the circadian clock in a manner similar to light. We tested the hypothesis that activation of excitatory amino acid (EAA) receptors in the SCN mediates the acute effects of light on Per1 mRNA levels and pineal melatonin. NMDA, injected into the SCN of Syrian hamsters during the night, acutely suppressed melatonin levels in the pineal gland. Both the NMDA receptor antagonist 2-amino-5-phosphonopentanoic acid (AP5) and the alpha-amino-3-hydroxy-5-methylisoxazoleproprionic acid (AMPA)/kainate receptor antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) inhibited the light-induced increase of Per1 mRNA levels in the SCN. In the same animals, however, these antagonists had no effect on the ability of light to suppress pineal melatonin. These results support the hypothesis that EAA receptor activation in the SCN is necessary for the acute effects of light on Per1 mRNA levels. They also indicate that NMDA receptor activation in the SCN is sufficient but may not be necessary for the acute effects of light on pineal melatonin. These data suggest that there may be at least two different neurochemical cascades that transduce the effects of light in the SCN
视交叉上核(SCN)包含一个生物钟,并调节松果体中褪黑素的合成。在主观夜间进行光照会急性增加SCN中周期蛋白(Per)1基因的mRNA水平,并急性抑制松果体中的褪黑素水平。已证明SCN中N-甲基-D-天冬氨酸(NMDA)受体的激活会以类似于光的方式使生物钟发生相位偏移。我们测试了以下假设:SCN中兴奋性氨基酸(EAA)受体的激活介导了光对Per1 mRNA水平和松果体褪黑素的急性影响。夜间将NMDA注射到叙利亚仓鼠的SCN中,可急性抑制松果体中的褪黑素水平。NMDA受体拮抗剂2-氨基-5-膦酰戊酸(AP5)和α-氨基-3-羟基-5-甲基异恶唑丙酸(AMPA)/海人酸受体拮抗剂6,7-二硝基喹喔啉-2,3-二酮(DNQX)均抑制了SCN中光诱导的Per1 mRNA水平的增加。然而,在同一动物中,这些拮抗剂对光抑制松果体褪黑素的能力没有影响。这些结果支持以下假设:SCN中EAA受体的激活对于光对Per1 mRNA水平的急性影响是必要的。它们还表明,SCN中NMDA受体的激活对于光对松果体褪黑素的急性影响是足够的,但可能不是必需的。这些数据表明,可能至少有两种不同的神经化学级联反应传导SCN中光的作用