Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors

L. Liu, W. Zhu, Z. S. Zhang, T. Yang, A. Grant, G. Oxford, S. A. Simon

Research output: Contribution to journalArticle

65 Citations (Scopus)

Abstract

Nicotine is an alkaloid that is used by large numbers of people. When taken into the body, it produces a myriad of physiological actions that occur primarily through the activation of neuronal nicotinic acetylcholine receptors (nAChRs). We have explored its ability to modulate TRPV1 receptors and voltage-gated sodium channels. The reason for investigating nicotine's effect on sodium channels is to obtain a better understanding of its anti-nociceptive properties. The reasons for investigating its effects on capsaicin-activated TRPV1 channels are to understand how it may modulate this channel that is involved in pain, inflammation, and gustatory physiology. Whole cell patch-clamp recordings from rat trigeminal ganglion (TG) nociceptors revealed that nicotine exhibited anesthetic properties by decreasing the number of evoked action potentials and by inhibiting tetrodotoxin-resistant sodium currents. This anesthetic property can be produced without the necessity of activating nAChRs. Nicotine also modulates TRPV1 receptors inducing a several-fold increase in capsaicin-activated currents in both TG neurons and in cells with heterologously expressed TRPV1 receptors. This sensitizing effect does not require the activation of nAChRs. Nicotine did nol alter the threshold temperature (∼41°C) of heat-activated currents in TG neurons that were attributed to arise from the activation of TRPV1 receptors. In this regard, its effect on TRPV1 receptors differs from those of ethanol that has been shown to increase the capsaicin-activated current but decrease the threshold temperature. These studies document several new effects of nicotine on channels involved in nociception and indicate how they may impact physiological processes involving pain and gustation.

Original languageEnglish (US)
Pages (from-to)1482-1491
Number of pages10
JournalJournal of Neurophysiology
Volume91
Issue number4
DOIs
StatePublished - Apr 2004
Externally publishedYes

Fingerprint

TRPV Cation Channels
Sodium Channels
Nicotine
Trigeminal Ganglion
Capsaicin
Nicotinic Receptors
Anesthetics
Physiological Phenomena
Voltage-Gated Sodium Channels
Neurons
Pain
Nociceptors
Temperature
Aptitude
Nociception
Tetrodotoxin
Evoked Potentials
Alkaloids
Action Potentials
Ethanol

ASJC Scopus subject areas

  • Physiology
  • Neuroscience(all)

Cite this

Liu, L., Zhu, W., Zhang, Z. S., Yang, T., Grant, A., Oxford, G., & Simon, S. A. (2004). Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors. Journal of Neurophysiology, 91(4), 1482-1491. https://doi.org/10.1152/jn.00922.2003

Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors. / Liu, L.; Zhu, W.; Zhang, Z. S.; Yang, T.; Grant, A.; Oxford, G.; Simon, S. A.

In: Journal of Neurophysiology, Vol. 91, No. 4, 04.2004, p. 1482-1491.

Research output: Contribution to journalArticle

Liu, L, Zhu, W, Zhang, ZS, Yang, T, Grant, A, Oxford, G & Simon, SA 2004, 'Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors', Journal of Neurophysiology, vol. 91, no. 4, pp. 1482-1491. https://doi.org/10.1152/jn.00922.2003
Liu, L. ; Zhu, W. ; Zhang, Z. S. ; Yang, T. ; Grant, A. ; Oxford, G. ; Simon, S. A. / Nicotine Inhibits Voltage-Dependent Sodium Channels and Sensitizes Vanilloid Receptors. In: Journal of Neurophysiology. 2004 ; Vol. 91, No. 4. pp. 1482-1491.
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