Coderre T J
Département de Médecine, Université de Montréal, Que., Canada.
Neurosci Lett. 1992 Jun 22;140(2):181-4. doi: 10.1016/0304-3940(92)90097-q.
This paper provides evidence that central sensitization and persistent nociception following formalin-induced tissue injury in rats is dependent on the production of protein kinase C. Persistent nociceptive behavior in rats induced by subcutaneous formalin injection was significantly reduced by intrathecal pretreatment with a phospholipase C inhibitor (neomycin), and an inhibitor of protein kinase C (W-7), and was significantly enhanced by a phorbol ester (phorbol 12-myristate 13-acetate, PMA) and a stimulator of protein kinase C (SC-10). It is expected that noxious inputs associated with tissue injury produce a release of aspartate and glutamate within the spinal dorsal horn which by acting at ionotropic (NMDA) and metabotropic excitatory amino acid receptors produce an increase in intracellular messengers such as calcium and diacylglycerol which stimulate protein kinase C.
本文提供的证据表明，大鼠福尔马林诱导的组织损伤后中枢敏化和持续性伤害感受取决于蛋白激酶C的产生。鞘内注射磷脂酶C抑制剂（新霉素）和蛋白激酶C抑制剂（W-7）可显著降低皮下注射福尔马林诱导的大鼠持续性伤害感受行为，而佛波酯（佛波醇12-肉豆蔻酸酯13-乙酸酯，PMA）和蛋白激酶C激活剂（SC-10）则可显著增强该行为。预期与组织损伤相关的伤害性输入会导致脊髓背角内天冬氨酸和谷氨酸的释放，它们通过作用于离子型（NMDA）和代谢型兴奋性氨基酸受体，使细胞内信使如钙和二酰甘油增加，从而刺激蛋白激酶C。
