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J Neurophysiol 89: 1387-1401, 2003; doi:10.1152/jn.00210.2002
0022-3077/03 $5.00
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J Neurophysiol (March 1, 2003). 10.1152/jn.00210.2002
Submitted on Submitted 20 March 2002; accepted in final form 19 November 2002

Modulation of IA Currents by Capsaicin in Rat Trigeminal Ganglion Neurons

L. Liu and S. A. Simon

Departments of Anesthesiology and Neurobiology, Duke University Medical Center, Durham, North Carolina 27710

Liu, L. and S. A. Simon. Modulation of IA Currents by Capsaicin in Rat Trigeminal Ganglion Neurons. J. Neurophysiol. 89: 1387-1401, 2003. When capsaicin, the pungent compound in hot pepper, is applied to epithelia it produces pain, allodynia, and hyperalgesia. We investigated, using whole cell path clamp, whether some of these responses induced by capsaicin could be a consequence of capsaicin blocking IA currents, a reduction in which, such as occurs in injury, increases neuronal excitability. In capsaicin-sensitive (CS) rat trigeminal ganglion (TG) neurons, capsaicin inhibited IA currents in a dose-dependent manner. IA currents were reduced 49% by 1 µM capsaicin. In capsaicin-insensitive (CIS) rat TG neurons, or small-diameter mouse VR1-/- neurons, 1 µM capsaicin inhibited IA currents 9 and 3%, respectively. These data suggest that in CS neurons the vast majority of the capsaicin-induced inhibition of IA currents occurs as a consequence of the activation of vanilloid receptors. Capsaicin (1 µM) did not alter the IA conductance-voltage relationship but shifted the inactivation-voltage curve about 15 mV to hyperpolarizing voltages, thereby increasing the number of inactivated IA channels at the resting potential. IA currents were relatively unaffected by 1 mM CTP-cAMP or 500 nM phorbol-12, 13-dibuterate (a protein kinase C agonist) but were inhibited by 20-30% with either 1 mM CTP-cGMP or 25 µM N-(6-aminohexyl)-5-chloro-1-napthalenesulfonamide HCl (a calcium-calmodulin kinase inhibitor). In the presence of 0.5 µM KT5823, an inhibitor of protein kinase G (PKG) pathways, 1 µM capsaicin inhibited IA by only 26%. In summary, in CS neurons, capsaicin decreases IA currents through the activation of vanilloid receptors. That activation, partially through the activation of cGMP-PKG and calmodulin-dependent pathways should result in increased excitability of capsaicin-sensitive nociceptors.




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