Effects of nicotine and tobacco smoke on the electrical activity of the cerebral cortex and olfactory bulb

Abstract

1 . Effects of nicotine, cigarette smoke and carbon monoxide have been compared in the cat encéphale isolé preparation, exhibiting a synchronized electrocorticogram (ECoG) and behavioural sleep. 2 . 2 ml samples of smoke, containing approximately 7 μg nicotine (approximately 2 μg nicotine/kg for a 3 kg cat), introduced into the lungs at 30 s intervals from a smoking simulator, caused desynchronization of the ECoG and behavioural arousal. 3 . Effects of smoke were matched in the same experiments by intravenous injections of nicotine, 2 μg/kg every 30 s. 4 . The use of specific nicotine antagonists, for example mecamylamine, and filters for removing nicotine, indicated the presence in smoke of other agents capable of exerting a pharmacological response. 5 . Cigarette smoke contains approximately 5·0% carbon monoxide. Introduced into the lungs of cats pretreated with mecamylamine (2 mg/kg), 2 ml samples of 5% carbon monoxide caused changes in the ECoG similar to those caused by smoke. 6 . Effects of nicotine or smoke were not modified by pretreatment with chlorpromazine (2·0–4·0 mg/kg). Atropine (0·3 mg/kg), however, prevented the cortical activation, but not the behavioural arousal. 7 . 2 ml samples of smoke applied to the nostrils caused the occurrence in the olfactory bulb of a discharge or burst of “induced” waves. This discharge was sometimes accompanied by a transient period of cortical activation. 8 . These studies demonstrate that in cats, nicotine is the principal pharmacological constituent of tobacco smoke as far as effects on the central nervous system are concerned, although other constituents of smoke may play a contributory role.