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Chronic IL-1 Signaling Potentiates Voltage-Dependent Sodium Currents in Trigeminal Nociceptive Neurons

¹Departments of Anesthesiology, ²Neurobiology and Center of Neuroengineering, and ³Neurology, and ⁴Center for Translational Neuroscience, Duke University Medical Center, Durham, North Carolina

Submitted 16 May 2005; accepted in final form 19 November 2005

The proinflammatory cytokine interleukin-1 (IL-1) mediates inflammation and hyperalgesia, although the underlying mechanisms remain elusive. To better understand such molecular and cellular mechanisms, we investigated how IL-1 modulates the total voltage-dependent sodium currents (I_Na) and its tetrodotoxin-resistant (TTX-R) component in capsaicin-sensitive trigeminal nociceptive neurons, both after a brief (5-min) and after a chronic exposure (24-h) of 20 ng/ml IL-1. A brief exposure led to a 28% specific (receptor-mediated) reduction of I_Na in these neurons, which were found to contain type I IL-1 receptors (IL-1RI⁺) on both their soma and nerve endings. In marked contrast, after a 24-h exposure, the total sodium current was specifically increased by 67%, without significantly affecting the TTX-R component. This potentiation of I_Na was suppressed in the presence of selective inhibitors of protein kinase C and G-protein–coupled signaling pathways, thereby suggesting that I_Na can be modulated through multiple pathways. In summary, the potentiation of I_Na through chronic IL-1 signaling in nociceptive sensory neurons may be a critical component of inflammatory-associated hyperalgesia.

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