2000 Fiscal Year Final Research Report Summary
MECHANISMS OF INTRASPINAL TRANSMISSION OF NOCICEPTIVE INFORMATIONS : QUANTITATIVE EVALUATION OF INTRACELLULAR CALCIUM ION CONCENTRATION
| Project/Area Number |
09307037
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| Research Category |
Grant-in-Aid for Scientific Research (A).
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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 | SAPPORO MEDICAL UNIVERSITY |
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Principal Investigator |
NAMIK Akiyoshi SAPPORO MEDICAL UNIVERSITY, ANESTHESIOLOGY, PROFESSOR, 医学部, 教授 (00136954)
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| Co-Investigator(Kenkyū-buntansha) |
OMOTE Keiichi SAPPORO MEDICAL UNIVERSITY, ANESTHESIOLOGY, ASSOCIATE PROFESSOR, 医学部, 助教授 (60185676)
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| Project Period (FY) |
1997 – 2000
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| Keywords | SPINAL CORD / DORSAL HORN / CALCIUM ION / PROSTAGLANDIN / NEUROPATHIC PAIN / INFLAMMATORY PAIN |
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| Research Abstract |
THE INFLAUX OF CALCIUM IONS HAVE A ROLE IN THE SPINAL PROCESSING OF NOCICEPTIVE INFORMATION FROM PERIPHERAL INFLAMMATION.WE MEASURED IINTRACELLULAR CALCIUM ION CONCENTRATION ([CA2+]I) OF THE SPINAL DORSAL HORN NEURONS IN A MODEL OF CARRAGEENAN-INDUCED INFLAMMATION AND EXAMINED THE RESPONSE OF ([CA2+]I) TO PGE2 AND THE EFFECT OF PROSTAGLANDIN RECEPTOR SUBTYPE EP1 ANTAGONIST.A TRANSVERSE SLICES OF LUMBAR SPINAL CORD WERE PRELOADED WITH FURA-2AM.IN LAMINA II-V OF THEH DORSAL HORN NEURONS ON THE INFLAMED SIDE SHOWED HIGHER ([CA2+]I) THAN THE CONTRALATERAL SIDE.THE RESPONSE OF ([CA2+]I) TO PGE2 WAS GREATER ON THE INFLAMED IN LAMINA III-IV.THE PGE2-INDUCED INCREMENT OF ([CA2+]I) WAS SUPPRESSED BY PERFUSION OF EP1 ANTAGONIST, ONO-8711. INFLAMMTION INDUCES NEURONAL SENSITIZATION TO PGE2 AT THE SPINAL DORSAL HORN, AND THE PGE2-INDUCED INCREMENT OF ([CA2+]I) IS MAINLY MEDIATED THROUGH THE ACTIVATION OF EP1 RECEPTOR.
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