Biochemical analysis of involvement of light and proto-oncogene in the plasticity of the suprachiasmatic nucleus

1.视交叉上核（SCN）的功能可塑性颅内注射2-脱氧-D-葡萄糖（2DG）和电刺激SCN后的高血糖症和高胰高血糖素血症在致盲后4 - 6周通过眼眶摘除术受到抑制，并在致盲后12周再次出现。在设盲后第4 - 6周，作为食物的蛋白质摄入也受到抑制。这些发现表明SCN参与能量代谢的调节机制，包括作为大量营养素的蛋白质选择，并且这种调节功能可能由视网膜神经输入到SCN来维持。在完整的大鼠中，光暴露升高交感神经系统的神经活动，抑制副交感神经系统的神经活动，并且在SCN的双侧病变后未观察到这些变化。这些事实也支持上述论点。SCN的形态可塑性在上述手术致盲动物中，SCN神经元弥散分布， ...更多信息 设盲后第5周，2DG和SCN刺激引起的高血糖消失时，可见少量、散在分布。但在盲法后10周，高血糖再次出现，SCN神经元密集。此外，先天性失明大鼠、遗传性小眼大鼠的SCN体积和神经元数量显著减少，这些大鼠对颅内注射2DG的高血糖和高胰高血糖素反应受损。SCN中的原癌基因产物在接受视网膜神经输入的SCN腹侧部，c-Fos的表达呈日变化，在12 h光照和12 h黑暗周期中，光周期开始前c-Fos的表达最低，暗周期开始前c-Fos的表达最高。在上述设盲动物中未观察到该每日变化。此外，2DG，这eliminating高血糖，和胰岛素，这eliminating低血糖，诱导Fos在SCN的表达。这些是否发生了，现在正在调查中。在室旁核和视上核的加压素能神经元中，c-Fos在禁水24小时后有明显表达。然而，这种c-Fos的表达以及血浆加压素浓度的升高在盲遗传性小眼大鼠中未观察到。这些事实表明SCN也参与体液的调节。在SCN中观察到TrkB。少

1. Functional plasticity of the suprachiasmatic nucleus (SCN)Hyperglycemia and hyperglucagonemia after the intracranial injection of 2-deoxy-D-glucose (2DG) and electrical stimulation of the SCN were suppressed on week 4 to 6 after blinding by orbital enucleation and were reappeared on week 12 after the blinding. The protein intake as food was also suppressed on week 4 to 6 after the blinding. These findings suggest that the SCN is involved in the regulatory mechanism of engergy metabolism including protein selection as a macronutrient, and that this regulatory function might be maintained by the retinal neural input to the SCN. In intact rats light exposure elevated the neural activity of the sympathetic nervous system and suppressed that of the parasympathetic nervous system, and these changes were not observed after bilateral lesions of the SCN. These facts also support the above suggestion.2. Morphological plasticity of the SCNIn the above surgically blind animals SCN neurons diffu … More sely and dispersedly located on week 5 after the blinding when the hyperglycemia by 2DG and SCN-stimulation disappeared. However, SCN neurons densely located on week 10 after the blinding when the hyperglycemia reappeared. Furthermore, the volume and neuronal number of the SCN was markedly reduced in congenitally blind rats, hereditarymicrophthalmic rats, which has impaired hyperglycemic and hyperglucagonemic responses to the intracranial injection of 2DG.3. Proto-oncogene products in the SCNExpression of c-Fos in the ventral part of the SCN which receives the retinal neural input showed a daily variation, and the lowest expression was observed just before the onset of the light period and the highest one just before the onset of the dark period under 12-h light and 12-h dark cycle. This daily variation was not observed in the above blind animals. Moreover, 2DG, which elicits hyperglycemia, and insulin, which does hypoglycemia,induced Fos expression in the SCN. Whether these were happens or not is now under the investigation. Marked expression of c-Fos was observed after water-deprivation for 24 hours in vasopressinergic neur ons of the paraventricular nucleus and the supraoptic nucleus. However, this c-Fos expression as well as the elevation of the plasma vasopressin concentration was not observed in the blind hereditary microphthalmic rats. These facts suggest that the SCN is also involved in the regulation of the body fluid. TrkB was observed in the SCN. Less