1994 Fiscal Year Final Research Report Summary
Involvement of Limbic System in Central Nervous System-Mediated Circulatory Regulation
| Project/Area Number |
04670529
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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 |
Circulatory organs internal medicine
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| Research Institution | Nagoya University |
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Principal Investigator |
ITOH Kenichi Nagoya University, School of Medicine Assistant Professor, 医学部, 助手 (80193481)
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| Co-Investigator(Kenkyū-buntansha) |
IGUCHI Akihisa Nagoya University, School of Medicine Professor, 医学部, 教授 (20109763)
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| Project Period (FY) |
1992 – 1994
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| Keywords | Limbic system / Blood pressure / Hippocampus / Cholinergic neurons / Anygdala / Sympathetic neurons / Desensitization / Neostigmine |
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| Research Abstract |
1. Circulatory regulation by limbic system
(1) Injection of neostigmine, acetylcholinesterase inhibitor, into the hippocampus in anesthetized rats induced a pressor resonse, which was suppressed by coadministration of pirenzepine. Bilateral adrenalectomy did not affect the pressor response. These results suggested that stimulation of M1 subtype muscarinic cholinergic neurons in rat hippocampus evokes a pressor response through activation of sympathetic nervous system to the heart and peripheral vasculature. (2) Injection of bucuculline (GABAA antagonist) into amygdala induced a pressor response. While bilateral adrenalectomy did not affect the pressor response, pretreatment of hexamethonium i.p.suppressed it. These results suggested that GABA-nergic neurons in amygdala play a role in inhibitory regulatory mechanisms via sympathetic drives to the heart and peripheral vasculature.
2. Desensitization mechanism of pressor responses by central nervous system stimulation
(1) Injection of neostigmine into the third cerebral ventricle in unanesthetized freely moving rats induced a pressor response. The responses by repeated stimulation of three times at four hour intervals were desensitized in bilateral adrenalectomized rats but not in intact rats. Increases of plasma norepinephrine were not desensitized in both groups of animals. These results suggested that adrenal gland have some role in antagonizing desensitization of pressor responses induced by repeated stimulation of central cholinergic neurons. (2) Increases of plasma epinephrine and hyperglycemic responses were desensitized by repeated intracerebroventricular injection of neostigmine. These evidences suggested that circulatory and metabolic responses by repeated stimulation of central nervous system were separately regulated and this dissociation reflected that of sympathoadrenal syatem.
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