1992 Fiscal Year Final Research Report Summary
Biochemical analysis of involvement of light and proto-oncogene in the plasticity of the suprachiasmatic nucleus
| Project/Area Number |
03670124
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
General medical chemistry
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| Research Institution | Osaka University |
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Principal Investigator |
NAGAI Katsuya Osaka University, Institute for Protein Research, Associate Professor, たんぱく質研究所, 助教授 (70029966)
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| Project Period (FY) |
1991 – 1992
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| Keywords | Suprachiasmatic nucleus / Plasticity / Light / Proto-oncogene / C-Fos / Trk / NGF / 2-deoxy-D-glucose |
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| Research Abstract |
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 SCN
In the above surgically blind animals SCN neurons diffu
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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 SCN
Expression 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
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