| Project/Area Number |
14571469
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Nippon Medical School |
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Principal Investigator |
TAKEDA Shinhiro Nippon Medical School, Assistant professor, 医学部, 講師 (00247008)
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| Co-Investigator(Kenkyū-buntansha) |
KIM Chol Nippon Medical School, Assistant professor, 医学部, 助手 (80318493)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2003: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | opioid / cannabinoid / membrane potential / respiratory center / Inspiratory neuron / Brainstem / Respiratory neuron |
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| Research Abstract |
Membrane potential and resistance (Rm) were measured in inspiratory neurons in rostral ventrolateral medulla (RVLM) of the isolated brainstem-spinal cord preparation from newborn rats during bath application of opioids (μ-receptor agonists) and cannabinoid (CB1 receptor agonist : WIN 55212-2). μ-opioid receptor agonist caused reduction of final motor outputs by mainly inhibiting medullary inspiratory neuron network. This inhibition of inspiratory neurons seems to be due to both a pre-and postsynaptic inhibition. The central respiratory rhythm as reflected by the preinspiratory neuron burst rate was essentially unaltered by the agonists. WIN 55212-2 did not induced respiratory depression. Respiratory rate did not also change after application of CB1 receptor antagonist. Respiratory rate was decreased after application of μ-opioid receptor agonist from 8.4±1.9 to 2.7±1.8 bursts/min. This opioid-induced respiratory depression was parcially reversed by WIN 55212-2 from 2.7±1.8 to 6.32±1.9 bursts/min.
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