Quantification of slow-wave EEG induced by atropine: effects of physostigmine, amphetamine and haloperidol

The goal of this study was to investigate whether the atropine-induced slow waves in the rat EEG could be easily quantified and used to assess the action of drugs on the central cholinergic systems manifested at the cortical level. Cable-transmitted EEG recordings were made in freely-moving male rats over periods of 5-6 h. Visual inspection of the EEG led us to divide it into 2 states, according to frequency and amplitude criteria: desynchronized, low voltage activity was termed 'State 1', also including other arousal patterns like 'theta spindles'. Slow-wave, high voltage activity, as well as faster patterns like spindles of slow-wave sleep, were included in 'State 2'. The time spent in State 2 (chosen because slow waves are admittedly increased by atropine) was visually determined on the EEG paper tracings. Atropine per se, at increasing doses, (1, 3, 10, 30 and 100 mg/kg i.p.), induced an increased duration of State 2. By contrast, physostigmine per se at doses of 0.01, 0.1 and 0.3 mg/kg i.p. reduced this duration with increasing doses. The atropine (10 mg/kg i.p.)-induced increase of State 2 was markedly attenuated by physostigmine (0.1 and 0.3 mg/kg i.p.) and amphetamine (1 mg/kg i.p.), but potentiated by haloperidol (0.3 mg/kg i.p.). The effects of the different drugs and combinations on the general behavior were also noted. In conclusion, this approach appears to present a promising tool for the study of the interaction of drugs with central cholinergic systems.