2006 Fiscal Year Final Research Report Summary
Role of glutamate receptors to develop abnormal pain following trigeminal nerve injury in awake behaving monkeys
| Project/Area Number |
17591952
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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 | Nihon University |
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Principal Investigator |
IWATA Koichi Nihon University, School of Dentistry, Professor, 歯学部, 教授 (60160115)
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| Co-Investigator(Kenkyū-buntansha) |
TSUBOI Yoshiyuki Nihon University, School of Dentistry, Assistant Professor, 歯学部, 講師 (50246906)
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| Project Period (FY) |
2005 – 2007
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| Keywords | awake behaving monkey / glutamate receptor / neuropathic pain / trigeminal nerve / capsaicin / N type calcium channel / trigeminal spinal nucleus |
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| Research Abstract |
Two major studies were conduced in the present project, 1) awake behaving monkey study and 2) anesthetized rat study.
1) In order to evaluate the neuronal mechanisms of abnormal pain in the trigeminal region, the effect of N type calcium channel blocker, ONO 2921 was systemically applied to the awake behaving monkeys with capsaicin induced hyperalgesia. The thermal detection task was trained in capsaicin treated monkeys. N type calcium was applied orally or via nasal membrane, and the thermal detection latency was measured. Heat detection latency was significantly elongated after ONO 2921 administration. The elongation of detection latency was slightly longer in oral-administrated monkeys compared with nasal-administrated monkeys. We could not any significant change in detection latency in capsaicin-untreated monkeys after ONO 2921 administration. The present results suggest that ONO 2921 have potent ability to reduce abnormal pain following capsaicin treatment in monkeys.
2) The rats' model with inferior orbital nerve injury was studied how the glutamate receptors were involved in the trigeminal neuropathic pain. Rats showed reduction of escape threshold to mechanical stimulation of the face following infra-orbital nerve (ION) injury. We observed significant enhancement of neuronal activity in the trigeminal spinal subnucleus caudalis (Vc) of the rats with ION ligation. After AMPA receptor antagonist CNQX caused significant reduction of neuronal activity in this rat, but not after NMDA receptor antagonist APV or MK801 administration. These suggest that AMAP receptor is involved in trigeminal abnormal pain following trigeminal nerve injury.
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