THE present study was designed to investigate the hypothesis that nico
tine may act via thalamic and basal forebrain nicotinic acetylcholine
receptors to suppress neocortical high voltage spindling and slow wave
s in awake rats. Loca microinfusions of a nicotinic acetylcholine rece
ptor agonist (nicotine 3, 10 and 30 mu g) or antagonist (mecamylamine
10 mu g) into the vicinity of the basal forebrain cholinergic projecti
on neurones of the nucleus basalis had no effect on cortical EEG waves
. However, nicotine (3, 10 and 30 mu g) microinfusions into the thalam
us decreased high voltage spindles and desynchronized non-spindling EE
G waves in the cortex. This suggests that nicotinic acetylcholine rece
ptor active drugs may modulate thalamocortical oscillations and desync
hronize EEG waves via brain stem cholinergic projections at the thalam
us.