Tobacco Smoking Can Potentiate C-fiber Evoked Potentials in Human Brain
Takahiro Miyazaki*, 1, 2, Xiaohong Wang1, Koji Inui1, 2, Edward F. Domino3, Ryusuke Kakigi1, 2
Identifiers and Pagination:Year: 2009
First Page: 71
Last Page: 75
Publisher Id: TOPAINJ-2-71
Article History:Received Date: 28/07/2009
Revision Received Date: 16/09/2009
Acceptance Date: 17/09/2009
Electronic publication date: 5/11/2009
Collection year: 2009
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The effects of smoking and nicotine on ultralate laser evoked potentials (LEPs), the EEG responses to C-fiber stimulation by a laser beam, were investigated in humans. Ultralate LEPs were repeatedly measured in two sessions, one after smoking, and the other in abstinence from smoking. The dominant frequency of the background EEG alpha activity, heart rate and venous plasma nicotine concentration were also measured. The peak-to-peak amplitude of the two major components (N2 and P2) of ultralate LEPs was significantly correlated both with the plasma nicotine concentration and with the background alpha frequency. The results suggest an arousal effect of nicotine on C-fiber mediated pain. The effect of nicotine on C-fiber LEPs was in the opposite direction of that on Aδ fiber LEPs. The difference between C and Aδ fibers might indicate a difference in effects of nicotine on first and second pain responses.