1998 Fiscal Year Final Research Report Summary
Mechanisms of deafferentation pain : examination in human and animal central nervous systems
| Project/Area Number |
09671433
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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 |
Cerebral neurosurgery
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| Research Institution | University of The Ryukyus School of Medicine |
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Principal Investigator |
YAMASHIRO Katsumi University of The Ryukyus School of Medicine, Department of Neurosurgery, assisstant professor, 医学部附属病院, 講師 (10124843)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIDA Akihiko University of The Ryukyus School of Medicine, Department of 2nd Anatomy, instruc, 医学部, 助手 (20295306)
HARAKUNI Tsuyoshi University of The Ryukyus School of Medicine, Department of Neurosurgery, instru, 医学部, 助手 (80295336)
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| Project Period (FY) |
1997 – 1998
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| Keywords | deafferentation pain / central nervous system / barbiturate / hyperactive neuron / calcium antagonist / NMDA receptor / GABA receptor |
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| Research Abstract |
Neurones with high- frequency dischargew ere found in the spinal dorsal horn and the thalamus of deaffer entation pain patients. We paid close attention to the high- frequency discharging neurones (hyper active neurones) in relation to deaffere ntation pain.
In human, prior to implantation of the deeps timulating electrodes, extracellular unitary activity was recorded by microelectrodes. A significant number of hyperactive neurones were recorded from the Vc nucleus. There were three types of discharge patterns in interval histograms. So me hyperactive neurones showed firing suppuression for a short time peri odb y intravenous administration of p henytoin a ndC alciuma ntagonist (Nicardipine).
In a nimal experiments, unilateral dorsal roots ectioning from C5 to Th1 were made in male Wistarr ats according to the method of Lombard et al(1979). A few months after the operation, hyperactive neurones were recorded from the thalamic nuclei and lemniscus medialis. The firing patterns and distri bution of hyperactive neurones were very similar to those of humans. These hyper active neurones were unaffected by electrical stimulation of t hen ucleus r aphe d or salis and I ocus c eruleus. A ppi cation of benzodiazepine an d barb it ur ate showed reduction of firing.
lontophoretical application of glutamate showed an in crease in firing. In contrast, GABA and NMDA antagonist MK- 801 showed remarkable firing suppression. These results suggest that hyperactive neurone may correlate with the glutamatergic, especially NMDA and GABA ergic receptor or fibers.
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