2007 Fiscal Year Final Research Report Summary
Study on the role of the primary afferent fibers in thedevelopment/maintenance of the intractable pain in the oro-facial region
| Project/Area Number |
18592030
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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 |
Functional basic dentistry
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| Research Institution | Ohu University |
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Principal Investigator |
YONEHARA Norifumi Ohu University, School of Pharmaceutical Sciences, Professor (70124534)
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| Co-Investigator(Kenkyū-buntansha) |
TAKEMURA Motohide Osaka University, Faculty of Dentistry, Associate professor (70192169)
SHINICHI Sugiyo Osaka University, Faculty of Dentistry, Assistant professor (90397688)
KOIKE Yuuichi Ohu University, School of Pharmaceutical Sciences, Professor (90109421)
TAKADA Yoshinobu Ohu University, School of Pharmaceutical Sciences, Professor (40119590)
ABE Kenji Ohu University, School of Pharmaceutical Sciences, Assistant Professor (60405991)
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| Project Period (FY) |
2006 – 2007
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| Keywords | Glutamate / Nitric oxide / Peripheral nerve injury / Microdialysis / Trigeminal nucleus caudalis / Allodynia / Nerve injury |
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| Research Abstract |
It is well known that the pathological pain states such as allodynia, hyperalgesia, and phantom pain can result after nerve injury or chronic inflammation. It is also recognized that an increase in the afferent impulse flow from damaged nerve areas enhances the activity of spinal dorsal horn neurons and produces pain. The activation of N-methyl-D-aspartate (NMDA) receptors in spinal dorsal horn neurons is widely regarded to be critical for the development and maintenance of the hyperalgesia induced by nerve injury.
Increasing evidence suggests that, at the site of the first synaptic relay of nociceptive pathway, activation of N-methyl-D-aspartate (NMDA) receptors modulates nociceptive transmission via a nitric oxide (NO) pathway. Therefore, to further clarify the central mechanisms underlying the peripheral nerve injury-induced pathological pain in the trigeminal system, this project examined influence of NO to the change in excitatory amino acids (EAAs) level in the superficial layer of subnucleus caudalis of the brain-stem trigeminal sensory nuclear complex (SpVc-I, II) following a ligation injury to the inferior alveolar nerves.
A very high EAAs release responses was observed immediately after the start of the perfusion in ligated animals compared with sham-operated rats. The EAA level evoked by application of the 40-V tooth pulp-stimulation or 1% capsaicin cream was significantly higher in the ligated animals than those in the sham-operated animals. This increase of EAAs level induced by capsaicin cream was inhibited by adding carboxy-PTIO, an NO scavenger, to the perfusate.
These results suggest that alterations in the stimulus-evoked raised EAA levels that occur in the site of the first synaptic relay of the dental pain pathway and which are expressed via endogenous NO, and which play an important role in development and/or maintenance of pathological pain states following dental peripheral nerve injury
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