Watkins L R, Milligan E D, Maier S F
Dept of Psychology & the Center for Neurosciences, University of Colorado at, Boulder, CO, USA.
Trends Neurosci. 2001 Aug;24(8):450-5. doi: 10.1016/s0166-2236(00)01854-3.
Pain is classically viewed as being mediated solely by neurons, as are other sensory phenomena. The discovery that spinal cord glia (microglia and astrocytes) amplify pain requires a change in this view. These glia express characteristics in common with immune cells in that they respond to viruses and bacteria, releasing proinflammatory cytokines, which create pathological pain. These spinal cord glia also become activated by certain sensory signals arriving from the periphery. Similar to spinal infection, these signals cause release of proinflammatory cytokines, thus creating pathological pain. Taken together, these findings suggest a new, dramatically different approach to pain control, as all clinical therapies are focused exclusively on altering neuronal, rather than glial, function.
与其他感觉现象一样,疼痛传统上被认为完全由神经元介导。脊髓胶质细胞(小胶质细胞和星形胶质细胞)会加剧疼痛,这一发现需要改变这种观点。这些胶质细胞表现出与免疫细胞相同的特征,即它们对病毒和细菌作出反应,释放促炎细胞因子,从而产生病理性疼痛。这些脊髓胶质细胞也会被来自外周的某些感觉信号激活。与脊髓感染类似,这些信号会导致促炎细胞因子的释放,从而产生病理性疼痛。综上所述,这些发现提示了一种全新的、截然不同的疼痛控制方法,因为目前所有的临床治疗都只专注于改变神经元功能,而非胶质细胞功能。