1998 Fiscal Year Final Research Report Summary
Phaimacological analysis of a novel NMDA receptor mediating synaptic responses involued in pain transmossion in the spinal cord
| Project/Area Number |
09680815
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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 |
神経・脳内生理学
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| Research Institution | Saga Medical School |
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Principal Investigator |
KUMAMOTO Eiichi Saga Medical School, Associate Professor, 医学部, 助教授 (60136603)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Megumu Saga Medical School, Full Professor, 医学部, 教授 (10140641)
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| Project Period (FY) |
1997 – 1998
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| Keywords | Spinal cord / Substantia gelatinosa / Pain / glutamate / Patch-clamp / Synaptic transmission |
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| Research Abstract |
It is thought that peripheral noxious information is transmitted through unmyclinated C-and thinly-myelinated Adelta-afferents to superficial dorsal horn, particularly substantia gelatinosa (SG, lamina II of Rexed) neurons, in the spinal cord, where the pain transmission is modulated. We examined what effects acutely or chronically pain-eliciting stimuli have on glutamatergic excitatory synaptic transmission by applying the blind whole-cell patch-clamp technique to SG neurons of an adult rat spinal cord slice to which the dorsal root is attached. The SG neurons exhibited not only a non-NMDA but also NMDA response by stimulating repetitively Adelta-afferents ; the latter of which is less sensitive to AP-5 or Mg^2^+ than reported in other central neurons (1). Capsaicin potentiated spontaneous transmitter release (2) while attenuating the amplitude of excitatory postsynaptic currents evoked in SG neurons by stimulating C-, but not Adelta-afferent fibers, for more than 30 min. SG neurons in rats inflamed by an intraplantar injection of complete Freund's adjuvant displayed synaptic transmissions different from those in naive rats. In inflamed rats, SG neurons receiving Abeta-afferent inputs decreased in number whereas those having A43-afferent inputs increased (3). These results demonstrate that glutamatergic transmissions in SG neurons are mediated by both non-NMDA and NMDA receptors and that these exhibit a plastic alteration following a pain stimulation. For example, capsaicin acts on specifically C-fibers, resulting in an inhibition of evoked transmission ; this would account for, at least in part, an analgesic action of capsaicin. Peripheral inflammation induces a reorganization of Abeta-afferents to the SG from deeper laminae ; this may partly contribute to the development of allodynia.
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