1993 Fiscal Year Final Research Report Summary
Brain stem pathway to control cerebral circulation from nucleus tractus solitarii and its neurotransmitter
| Project/Area Number |
04670051
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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 physiology
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| Research Institution | University of Occupational and Environmental Health (1993)
Osaka City University (1992) |
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Principal Investigator |
MAEDA Masanobu University of Occupational Associate and Environmental Health, Proffessor Institute of Industrial Ecological Sciences, 産業生態科学研究所, 助教授 (80181593)
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| Project Period (FY) |
1992 – 1993
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| Keywords | Nucleus tractus solitarii / Ventrolateral medulla / Cerebrovascular circulation / Cardiovascular center / Neural pathway / N-methyl-D-aspartic acid (NMDA) / Neurotransmitter / Cardiovascular regulation |
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| Research Abstract |
N-methyl-D-aspartic acid (NMDA) was microinjected into the nucleus tractus solitarii (NTS) of urethane-anesthetized, paralyzed and artificially ventilated rats, and cerebral blood flow (CBF) was determined using a combination of labeled microspheres. The CBF in the cerebral cortex ipsilateral to the stimulated NTS significantly (P<0.01) decreased (n=9). The cerebrovascular resistance (CVR) in the cerebral cortex ipsilateral to the stimulated NTS significantly (p<0.01) increased. Blockade of NMDA receptors in the NTS abolished the CBF decrease and CVR increase responses elicited by microinjection of the NMDA into the NTS (n=9). Blockade of non-NMDA receptors in the NTS had little effect on the CBF decrease and CVR increase responses (n=10). These results suggest that the NMDA receptors in the NTS may be involved in the control of cerebral circulation.
Microinjection of L-glutamate (1.7nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (p<0.01) decrease in CBF and significant (P<0.01) increase in CVR in the cerebral cortex ipsilateral to the stimulated VLDA side (n=9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n=10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase responses following chemical stimulation of VLDA (n=11). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.
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