Long-term IL-1β exposure causes subpopulation-dependent alterations in rat dorsal root ganglion neuron excitability

Stemkowski PL, Smith PA. Long-term IL-1 beta exposure causes subpopulation-dependent alterations in rat dorsal root ganglion neuron excitability. J Neurophysiol 107: 1586-1597, 2012. First published December 14, 2011; doi:10.1152/jn.00587.2011.-The effect of interleukin-1 beta (IL-1 beta) on the electrical properties of sensory neurons was assessed at levels and exposure times comparable to those found in animal models of neuropathic pain. Experiments involved whole cell current-clamp recordings from rat dorsal root ganglion (DRG) neurons in defined-medium, neuron-enriched cultures. Five-to six-day exposure to 100 pM IL-1 beta produced subpopulation-dependent effects on DRG neurons. These included an increase in the excitability of medium-diameter and small-diameter isolectin B-4 (IB4)-positive neurons that was comparable to that found after peripheral nerve injury. By contrast, a reduction in excitability was observed in large-diameter neurons, while no effect was found in small-diameter IB4-negative neurons. Further characterization of changes in medium and small IB4-positive neurons revealed that some, but not all, effects of IL-1 beta were mediated through its receptor, IL-1RI. Although the acute actions of IL-1 beta on sensory neurons have been well studied and related to acute and/or inflammatory pain, the present study shows how sensory neurons respond to long-term cytokine exposure. Such effects are relevant to understanding processes that contribute to the onset of neuropathic pain.