Increased Sensitivity of Sensory Neurons to Tumor Necrosis Factor in Rats With Chronic Compression of the Lumbar Ganglia

Liu, Baogang, Huiqing Li, Sorin J. Brull, and Jun-Ming Zhang. Increased sensitivity of sensory neurons to tumor necrosis factor in rats with chronic compression of the lumbar ganglia. J Neurophysiol 88: 1393–1399, 2002; 10.1152/jn.00021.2002. Proinflammatory cytokines may sensitize primary sensory neurons and facilitate development of neuropathic pain processes after peripheral nerve injury. The goal of this study was to determine whether responses of dorsal root ganglion (DRG) neurons to exogenous tumor necrosis factor (TNF) are altered in a chronically compressed DRG (CCD) injury model. Extracellular recordings from teased dorsal root microfilaments demonstrated that acute topical application of TNFto the DRG for 15 min evoked Cand A -fiber responses in both normal and CCD rats. However, the response latency was significantly shorter, and the peak discharge rate was higher, in CCD fibers than in normal fibers. Intracellular recordings from smalland large-sized neurons showed that TNFinduced greater depolarization and greater decrease in rheobase in CCD neurons than in normal neurons. The proportion of both smalland large-sized neurons that were responsive to TNFincreased significantly after CCD injury. Furthermore, TNFaltered the discharge patterns of large, spontaneously active neurons in addition to enhancing their discharge rates. However, the depolarization caused by TNFin such neurons was minor ( 2 mV). Inflammatory cytokines such as TNFincreased the sensitivity of sensory neurons in normal and CCD rats. The CCD injury itself, on the other hand, increased neuronal responses to inflammatory cytokines.