| Project/Area Number |
07457351
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Niigata University |
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Principal Investigator |
BABA Hiroshi Niigata University, School of Medicine, Assistant, 医学部, 助手 (00262436)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Megumu Saga Medical School, School of Medicine, Professor, 医学部, 教授 (10140641)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥6,300,000 (Direct Cost: ¥6,300,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1995: ¥4,200,000 (Direct Cost: ¥4,200,000)
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| Keywords | adult rat / descending pain control / spinal cord slice / substantia gelatinosa / serotonine / noradrenaline / acetylcholine / whole cell patch clamp / 下行性疼痛抑制路 / ムスカリンレセプター |
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| Research Abstract |
Whole cell patch clamp recordings were made from substantia gelatinosa (SG) neurons to investigate the mechanisms of descending pain control systems in spinal cord level.
In the majority of SG neurons, serotonine (5-HT), noradrenaline (NA) and acetylcholine (ACh) evoked outward currents by increasing potassium conductance. These effects were mediated by 5-HTIA alpha2 and muscarinic receptors, respectively.
NA,5-HT and ACh increased the frequency of spontaneous IPSCs. The effects of NA and ACh were mediated by alpha1 and muscarimic receptors, respectively. The receptor subtype involed in 5-HT action was not clear. These effects were partially blocked by TTX,especially large amplitude of IPSCs were eliminated by TTX,suggesting that a portion of these IPSCs were results from soma-dendritic spiking.
NA,5-HT and ACh increased the frequency of miniature-IPSCs in the presence of TTX,suggesting thar NA,5-HT and ACh increase inhibitory transmitter release through presynaptic mechanism. The effects of NA and ACh were mediated by alpha1 and muscarinic receptors, respectively. The receptor subtype involved in 5-HT action was not clear.
These results indicate that there are at least two mechanisms by which the descending pain control systems inhibit SG neuros : 1) hyperpolarization through activation of K conductance ; 2) activation of GABA and glycine-containing inhibitory interneurons through pre-and postsynaptic mechanisms.
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