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

1.眼内注射2-脱氧-D-葡萄糖(2DG)和电刺激视交叉上核(SCN)后4~6周，视交叉上核(SCN)高血糖、高血糖及电刺激SCN的功能可塑性受到抑制，致盲后12周恢复正常。致盲后4~6周，作为食物的蛋白质摄入量也受到抑制。这些发现表明，SCN参与了能量代谢的调节机制，包括作为一种常量营养素的蛋白质选择，这种调节功能可能由SCN的视网膜神经输入来维持。在正常大鼠，光暴露增强了交感神经系统的神经活动，抑制了副交感神经系统的神经活动，而双侧毁损SCN后，这些变化没有观察到。这些事实也支持上述建议。上述手术致盲动物脊髓核神经元的形态可塑性扩散…致盲后5周，2DG和SCN刺激所致的高血糖消失时，更密集和分散。但在致盲后10周，当高血糖再次出现时，SCN神经元密集分布。此外，先天性盲大鼠、遗传性微眼症大鼠的SCN体积和神经元数量显著减少，这削弱了对脑内注射2DG.3的高血糖和高血糖反应。原癌基因产物在接受视网膜神经输入的SCN腹侧部分c-Fos的表达呈现日变化，在12h光照和12h暗周期下，在光期开始前表达最低，在暗期开始前表达最高。在上述盲目动物中没有观察到这种每日变化。此外，引起高血糖的2DG和引起低血糖的胰岛素可诱导SCN中Fos的表达。这些事件是否发生，目前正在调查中。缺水24小时后，c-Fos在室旁核和视上核的加压素能神经元有明显表达。然而，这种c-Fos的表达以及血浆血管加压素浓度的升高在失明遗传性小眼症大鼠中没有观察到。这些事实表明，SCN也参与了体液的调节。在SCN中观察到TrkB。较少

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