MECHANISMS OF INTRASPINAL TRANSMISSION OF NOCICEPTIVE INFORMATIONS : QUANTITATIVE EVALUATION OF INTRACELLULAR CALCIUM ION CONCENTRATION

伤害性信息的椎管内传递机制：细胞内钙离子浓度的定量评估

• 批准号: 09307037
• 负责人: NAMIK Akiyoshi
• 金额: $ 11.65万
• 依托单位: SAPPORO MEDICAL UNIVERSITY
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (A).
• 财政年份: 1997
• 资助国家: 日本
• 起止时间: 1997 至 2000
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-09307037/
• 关键词: SPINAL CORD; DORSAL HORN; CALCIUM ION; PROSTAGLANDIN; NEUROPATHIC PAIN; INFLAMMATORY PAIN; 疼痛; 細胞内カルシウム; プロスタグランディン; 病的疼痛; 細胞内カルシウムイオン; グルタミン酸; 脊髄後角細胞; 興奮性アミノ酸

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.

钙离子的流入在脊髓处理来自外周炎症的伤害性信息中起作用。在卡拉胶诱导的炎症模型中，我们测量了脊髓背角神经元细胞内钙离子浓度（[ca2 +] i），并检测了（[ca2 +] i）对pge2的反应和前列腺素受体亚型ep1拮抗剂的作用。用fura-2am预压腰椎脊髓横切片。在背角ii-v层，炎症侧的神经元（[ca2 +] i）高于对侧。（[ca2 +] i）对pge2的反应在iii-iv层的炎症反应更大。灌注ep1拮抗剂ono-8711可抑制pge2诱导的（[ca2 +] i）的增加。炎症诱导脊髓背角神经元对pge2致敏，pge2诱导的（[ca2 +] i）增加主要通过激活ep1受体介导。

项目成果

Kawamata T,Omote K: "The activation of spinal NMDA receptors stimulates a nitric oxide/cyclic guanosine 3', 5'-monophosphate/glutamate release cascade in nociceptivesignelling"Anesthesiology. 91. 1415-1424 (1999)

Kawamata T，Omote K：“脊髓 NMDA 受体的激活刺激伤害性信号中的一氧化氮/环鸟苷 3, 5-单磷酸/谷氨酸释放级联”麻醉学。

表圭一: "疼痛治療の現状と展望1998,38-56"ミクス. 234 (1998)

Keiichi Omote：“疼痛治疗的现状和前景 1998, 38-56” Mix 234 (1998)

表圭一、並木昭義: "帯状疱疹の診断と治療" 真興交易医書出版部, 264 (1998)

表敬一、并木明吉：《带状疱疹的诊断和治疗》新光贸易医学出版部，264（1998）

Yamauchi M: "Direct evidence for the role of nitric oxide on the gltcrnate-induced reuronal death in cultured contical neurons" Brain Research. (in press). (1998)

Yamauchi M：“一氧化氮对培养的视网膜神经元中谷氨酸诱导的肾细胞死亡的作用的直接证据”大脑研究。

Keiichi Omote and Akiyoshi Namiki: "Activation of peripheral NMDA-nitric oxide cascade in formalin test"Anesthesiology. 93(in press). (2000)

Keiichi Omote 和 Akiyoshi Namiki：“福尔马林试验中外周 NMDA-一氧化氮级联的激活”麻醉学。