Effects of tobacco smoking and abstinence on middle latency auditory evoked potentials*

Abstract

The shorter latencies of the middle latency brain wave components in the smoking session suggest faster processing of sensory information after cigarette smoking. Larger Pa amplitudes after cigarette smoking suggest a higher arousal level than that among partially abstinent smokers and nonsmokers.

Mouse model predicts effects of smoking and varenicline on event-related potentials in humans

“…Varenicline increased P20 amplitude in mice and P50 amplitude during abstinence in humans. Changes in EEG power and ERP amplitude are thought to reflect changes in arousal (Kishimoto & Domino, 1998;Pickworth, Herning, & Henningfield, 1989). Because decreased arousal is a symptom of nicotine withdrawal, varenicline's effects on sensory habituation may contribute to its therapeutic efficacy.…”

“…For example, nonpsychiatric heavy smokers exhibit greater P50 amplitude and S2:S1 ratio compared with never-smokers (Crawford et al). However, studies of the acute effects of smoking versus abstinence on P50 responses in normal smokers have yielded mixed results, with some studies demonstrating that the effects of smoking are mediated by S1 response (Adler et al, 1993;Crawford et al;Domino, 2003;Kishimoto & Domino, 1998).…”

Neonatal nicotine exposure impairs nicotinic enhancement of central auditory processing and auditory learning in adult rats

“…In humans, systemic nicotine (or tobacco smoking) has little effect on latency measures or on most amplitude measures of function in the auditory periphery (otoacoustic emissions) and brainstem auditory pathways (auditory brainstem response), but affects multiple latency and amplitude measures of auditory forebrain function (e.g. middle and long latency potentials) (Knott, 1987; Kishimoto & Domino, 1998; Harkrider & Champlin, 2001a, b; Harkrider et al ., 2001). Thus, at least under some conditions, cortical nAChRs may mediate most effects of systemic nicotine measured in A1 (but see text below on regulation of onset latency).…”

Nicotinic Acetylcholine Receptors in Sensory Cortex: Figure 1

“…In smokers, smoking increased the amplitude of longlatency visual (flash)-evoked potentials, whereas abstinence from smoking for many hours reduced the evoked potential amplitude (Hall et al 1973;Friedman and Meares 1980). Similarly, in the auditory system, smoking increased the amplitude and reduced the peak latency of middle latency (midbrain and forebrain) components of an auditory (click)-evoked potential relative to the response obtained following a period of abstinence, or relative to the response in nonsmokers (Kishimoto and Domino 1998; but see Friedman and Meares 1980). Earlier latency (brainstem) components of the auditory-evoked potential appeared unaffected by smoking or abstinence.…”