The Cholinergic Basis of the Smoking-Induced EEG Activation Profile

Abstract

Acute quantitative electroencephalographic effects of cigarette smoking were examined in 15 smokers within a repeated-measures design which assessed changes in power-spectral estimates following acute pre-treatment with placebo, a dose (20 mg) of mecamylamine, a dose (0.6 mg) of scopolamine and a combined dose of mecamylamine and scopolamine. Compared to sham smoking, the smoking of a single cigarette following placebo pre-treatment reduced absolute and relative power in slow (delta, theta) frequency bands, increased absolute and relative power in alpha and beta frequency bands and accelerated mean frequency. These smoking-induced power changes in slow- and fast-frequency bands were differentially affected by the separate and combined actions of the cholinergic antagonists with treatments involving mecamylamine tending to abolish smoking-induced slow-frequency absolute power reductions and fast-frequency relative power increments. Self-ratings of smoking-induced increases in alertness were altered by mecamylamine and combined treatments while sensory aspects of cigarette smoking were only altered with combined mecamylamine and scopolamine pre-treatment. The results are discussed with respect to brain-behaviour relationships and mechanisms maintaining the smoking habit.

Effects of Haloperidol Pretreatment on the Smoking-Induced EEG/Mood Activation Response Profile

“…Post-placebo/haloperidol assessments were collected after sham smoking and cigarette smoking, with sham smoking always preceding cigarette smoking. Although the non-randomization of sham and cigarette smoking confounds a time effect within each test session day with the smoking effect, the consecutive EEG assessments of sham and cigarette smoking effects were chosen for this exploratory study design in order to relate observations with our previous cholinergic blockade study which also utilized a nonrandomized sham versus cigarette smoking sequence [17].…”

“…It utilized bipolar analogue scales to examine 'sensory' aspects of smoke inhalation as well as general liking of the cigarette [17]. Specifically, the scales examined 'effects on throat' (too little -too much) and general liking (likedislike), smoothness (too smooth -too rough), hotness (too hot -too cool) and ease of draw (too easy -too hard).…”

“…Although both nicotinic and muscarinic acetylcholine receptors have been indicated in the regulation of EEG activation [11][12][13][14][15][16], muscarinic pretreatment with scopolamine failed to exert blocking actions on the smoking-induced EEG activation profile, while pretreatment with mecamylamine, alone or in combination with scopolamine, abolished smoking-induced slow (‰, ) frequency (absolute power) reductions and fast (· 2 , ß) frequency (relative power) increments [17]. Failure of cholinergic antagonists to completely antagonize all components of the smokinginduced EEG activation profile suggests that the electrocortical response to smoking may be mediated by more than one transmitter system.…”

Using Electrophysiological Measures to Assess the Consumer Acceptability of Smokeless Tobacco Products

“…36 Additionally, one of the most consistent electrophysiological changes following tobacco use is an alpha band activity change, reflecting either global alpha suppression, 19,21,20 or selective suppression of low alpha (8-10 Hz) 18 and/or increases in high alpha (12)(13)(14). [37][38][39] It should be noted that while the current investigation is not the first to identify alpha suppression across the 8-12 Hz alpha band in response to tobacco product use, 19,21,20 recently, it has been more common to identify selective suppression of low alpha (8-10 Hz) 18 and/or increases in high alpha (12)(13)(14). [37][38][39] Given that peak alpha frequency is known to vary across individuals, 40 the subtle differences in terms of the alpha effects observed across studies may be due to differences in the average peak alpha frequency of the participants included in a given sample.…”

“…[37][38][39] It should be noted that while the current investigation is not the first to identify alpha suppression across the 8-12 Hz alpha band in response to tobacco product use, 19,21,20 recently, it has been more common to identify selective suppression of low alpha (8-10 Hz) 18 and/or increases in high alpha (12)(13)(14). [37][38][39] Given that peak alpha frequency is known to vary across individuals, 40 the subtle differences in terms of the alpha effects observed across studies may be due to differences in the average peak alpha frequency of the participants included in a given sample. Additionally, differences in the present report may be due to the fact that our investigation employed an eyes-open resting state methodology.…”