2006 Fiscal Year Final Research Report Summary
Is the hypothalamic paraventricular nucleus-locus coeruleus neuronal circuit involved in persistent increase in the plasma cortisol?
| Project/Area Number |
17591217
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Psychiatric science
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| Research Institution | Kochi University |
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Principal Investigator |
OKADA Shoshiro Kochi University, Pharmacology, associate professor, 医学部, 助教授 (40203989)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Naoko Kochi University, Pharmacology, assistant professor, 医学部, 助手 (50380324)
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| Project Period (FY) |
2005 – 2006
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| Keywords | hypothalamic paraventricular nucleus / locus coeruleus / noradrenaline / corticotropin releasing factor (CRF) / nicotinic receptor α3 subunit / cFos / CRF1 receptor / ニコチン受容体 |
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| Research Abstract |
The present study was undertaken to clarify the central mechanisms, involved in the intracerebroventricularly administered corticotropin-releasing factor-induced elevation of plasma corticosterone in urethane- and α-chloralose-anesthetized rats using microdialysis and immunohistochemical techniques. When corticotropin-releasing factor was given at 0.5,1.5,and 3.0 nmol/animal intracerebroventricularly, it dose-dependently increased noradrenaline release but not adrenaline release in the hypothalamic paraventricular nucleus. The 1.5 nmol/animal dose of corticotropin-releasing factor-induced noradrenaline release was attenuated by CP-154,526 (butyl-ethyl-{2,5-dimethy1-7-(2,4,6trimethylpheny1)-7H-pyrrolo [2,3-d] pyrimidin-4-yl} amine), a selective corticotropin-releasing factor 1 receptor antagonist, at 1.3 mol/animal, intracerebroventricularly, and was also abolished by phentolamine at 0.66 mol/animal, intracerebroventricularly. In addition, the corticotropin-releasing factor-induced elev
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ation of noradrenaline release in-the hypothalamic paraventricular nucleus and plasma corticosterone were abolished by hexamethonium, a nonselective nicotinic acetylcholine receptor antagonist, at 1.8 μmol/animal, intracerebroventricularly, and α-conotoxin MII, a potent α_3β_2 nicotinic acetylcholine receptor antagonist, at 30 nmol/animal, i.c.v. Corticotropin-releasing factor at 1.5 nmol/animal, i.c.v. evoked a significant expression of cFos, an immediate-early gene product, on the dopamine-β-hydroxylase-containing neurons and α_3 nicotinic acetylcholine receptor subunit-expressing neurons in the locus coeruleus, but not in the medullary A_1 and A_2 regions containing noradrenergic neurons. These results suggest that centrally administered corticotrophin-releasing factor elevates plasma corticosterone by the corticotropin-releasing factor 1 receptor and α_3 subunit-containing nicotinic acetylcholine receptor (probably α_3 β_2 nicotinic acetylcholine receptor) mediated activation of the locus coeruleus noradrenergic neurons projecting to the paraventricular nucleus in rats Less
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