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Femoral artery occlusion in rats has been used to study human peripheral artery disease (PAD). Using this animal model, a recent study suggests that increases in levels of tumor necrosis factor-α (TNF-α) and its receptor lead to exaggerated responses of sympathetic nervous activity and arterial blood pressure as metabolically sensitive muscle afferents are activated. Note that voltage-dependent Na +  subtype Na V 1.8 channels (Na V 1.8) are predominately present in chemically sensitive thin fiber sensory nerves. The purpose of this study was to examine the role played by TNF-α in regulating activity of Na V 1.8 currents in muscle dorsal root ganglion (DRG) neurons of rats with PAD induced by femoral artery occlusion. DRG neurons from control and occluded limbs of rats were labeled by injecting the fluorescent tracer DiI into the hindlimb muscles 5 days before the experiments. A voltage patch-clamp mode was used to examine TTX-resistant (TTX-R) Na V  currents. Results were as follows: 72 h of femoral artery occlusion increased peak amplitude of TTX-R [1,922 ± 139 pA in occlusion ( n = 11 DRG neurons) vs. 1,178 ± 39 pA in control ( n = 10), means ± SE; P &lt; 0.001 between the 2 groups] and Na V 1.8 currents [1,461 ± 116 pA in occlusion ( n = 11) and 766 ± 48 pA in control ( n = 10); P &lt; 0.001 between groups] in muscle DRG neurons. TNF-α exposure amplified TTX-R and Na V 1.8 currents in DRG neurons of occluded muscles in a dose-dependent manner. Notably, the amplification of TTX-R and Na V 1.8 currents induced by TNF-α was attenuated in DRG neurons with preincubation with respective inhibitors of the intracellular signaling pathways p38-MAPK, JNK, and ERK. In conclusion, our data suggest that Na V 1.8 is engaged in the role of TNF-α in amplifying muscle afferent inputs as the hindlimb muscles are ischemic; p38-MAPK, JNK, and ERK pathways are likely necessary to mediate the effects of TNF-α.

american journal of physiology. regulatory, integrative and comparative physiology/american journal of physiology. regulatory, integrative, and comparative physiology

Enhancement by TNF-α of TTX-resistant NaV current in muscle sensory neurons after femoral artery occlusion

Enhancement by TNF-α of TTX-resistant Na_V current in muscle sensory neurons after femoral artery occlusion