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

Ca ~（2+）离子在脊髓对周围性炎症伤害性信息的加工过程中起一定作用。我们测定了角叉菜胶诱发的脊髓背角炎症模型神经元细胞内Ca ~（2+）浓度（[Ca ~（2+）]I），并观察了[Ca ~（2+）]I的反应。前列腺素受体亚型EP 1拮抗剂对前列腺素E_2的影响炎侧背角神经元的[Ca ~（2+）]I高于炎侧背角神经元的[Ca ~（2+）]I，炎侧背角神经元的[Ca ~（2+）]I对PGE_2的反应性高于炎侧背角神经元的[Ca ~（2+）] i，给予EP_1拮抗剂ONO-8711可抑制PGE_2引起的[Ca ~（2+）] i升高。炎症诱导脊髓背角神经元对PGE 2的敏感化，PGE 2诱导的（[Ca 2 +]I）增加主要通过激活EP 1受体介导。

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.