1997 Fiscal Year Final Research Report Summary
Investigation to mechanisms of the generation of hyperalgesia following nerve injury
| Project/Area Number |
08671718
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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 | Niigata University |
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Principal Investigator |
TOMITA Misao Niigata University Hospital Assistant, 医学部・附属病院, 助手 (60221438)
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| Co-Investigator(Kenkyū-buntansha) |
YOSHIMURA Megumu Saga Medical College School of Medicine Professor, 医学部, 教授 (10140641)
BABA Hiroshi Niigata University School of Medicine Assistant, 医学部, 助手 (00262436)
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| Project Period (FY) |
1996 – 1997
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| Keywords | spinal cord slice / visualized membrane potential / substantia gelatinosa / chronic pain model / voltage sensitive dye / sciatic nerve transection / whole cell patch clamp |
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| Research Abstract |
Plastic changes in sensory pathways in the spinal dorsal horn have been suggested to be a possible underlying mechanism for hyperalgesia following peripheral nerve injury, which is a common cause of human suffering. Supportive evidence has emerged from recent morphological studies that following peripheral nerve injury Abeta afferents, which normally convey innocuous information to deeper laminae (laminae III-VI), sprout into lamina II (substantia gelatinosa), a region which preferentiallyreceives nociceptive inputs from Adelta and C afferents under normal conditions. It is not clear, however, whether the redirected Abeta afferents establish functional connections in, and transmit sensory information to, the newly innervated region. We demonstrate, using spina cord slices from sciatic nerve transected rats, that mono-and poly-synaptic responses are elicited in substantia gelatinosa neurons by stimulation of Abeta afferents. These observations suggest that tactile information conveyed by Abeta afferents is directly, or indirectly, transmitted to the substantia gelatinosa. This functional reorganization in the sensory circuitry may be responsible for pathological pain states such as allodynia in humans.
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