Riekkinen P, Kuitunen J, Riekkinen M
Department of Neurology, University of Kuopio, Finland.
Neuroreport. 1995 Aug 21;6(12):1625-8. doi: 10.1097/00001756-199508000-00009.
The present study was designed to investigate the hypothesis that nicotine may act via thalamic and basal forebrain nicotinic acetylcholine receptors to suppress neocortical high voltage spindling and slow waves in awake rats. Loca microinfusions of a nicotinic acetylcholine receptor agonist (nicotine 3, 10 and 30 micrograms) or antagonist (mecamylamine 10 micrograms) into the vicinity of the basal forebrain cholinergic projection neurones of the nucleus basalis had no effect on cortical EEG waves. However, nicotine (3, 10 and 30 micrograms) microinfusions into the thalamus decreased high voltage spindles and desynchronized non-spindling EEG waves in the cortex. This suggests that nicotinic acetylcholine receptor active drugs may modulate thalamocortical oscillations and desynchronize EEG waves via brain stem cholinergic projections at the thalamus.