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Anticholinergic drugs have been proposed as possible acute model for investigating geriatric-associated cognitive deficits, but the interactive effect of muscarinic and nicotinic cholinergic blockade on cognitive processes has yet to be examined. Behavioural performance and P300 event-related potential (ERP) measures were assessed in visual and auditory continuous performance (CPT) takes in 10 young adults before and after the double-blind acute administration of a placebo, a centrally acting nicotinic blocker (20 mg mecamylamine), a centrally acting muscarinic blocker (0·6 mg scopolamine) and a combination dose of mecamylamine and scopolamine. Relative to placebo, single and combined drug administration failed to alter response accuracy, but slowed reaction times in both tasks and decreased subjective alertness. Mecamylamine along significantly reduced P300 amplitudes, but only during the visual CPT. The results are discussed in relation to cholinergic functioning in normal and pathological cognition. Copyright © 1999 John Wiley & Sons, Ltd.

Anticholinergic drugs have been proposed as a possible acute model for human electroencephalographic (EEG) studies focused on dementia but the interactive effects of muscarinic and nicotinic cholinergic receptor system blockade on the regulation of electrocortical activity has yet to be examined. EEG recordings were carried out in 15 normal subjects before and after the double-blind acute administration of a placebo, a centrally acting nicotinic blocker (20 mg of mecamylamine), a centrally acting muscarinic blocker (0·6 mg of scopolamine) and a combination dose of mecamylamine and scopolamine. Mecamylamine decreased absolute and relative beta power and increased relative theta power. Scopolamine increased relative power in both theta and beta frequency bands. Mecamylamine produced greater theta increments than scopolamine, while combined administration of the two central blockers induced changes similar to that observed with mecamylamine administered alone. Results are discussed in relation to electrocerebral activity in normal and pathological aging. © 1997 John Wiley & Sons, Ltd.