Abstract
Statistical analysis of EEG spectra averaged over 10-min intervals showed that in rats performing free behavior, peripheral administration of the acetylcholinesterase inhibitor physostigmine induced long-lasting characteristic changes (lasting tens of minutes) in the electrical activity of the dorsal hippocampus (field CAI) and the somatosensory cortex. An increase in the physostigmine dose from 0.05 to 1 mg/kg shifted the peak of the theta rhythm to lower frequencies (3.6-4.9 Hz) without a change in power at this frequency, though there was a decrease in power at 5.7-11.9 Hz. The power of the beta-1 rhythm (13.8-16.4 Hz) was also strongly suppressed. In contrast, the power of the beta-2 rhythm (20.3-26.5 Hz) increased several-fold in a non-linear fashion. Scopolamine suppressed all the changes induced by physostigmine, demonstrating the important role of m-cholinoceptors in changes in EEG spectra. The high dose of physostigmine caused inversion of the power of the beta-2 rhythm: unlike the situation obtaining in controls, the beta-2 power in the hippocampus became significantly greater than that in the neocortex. These data suggest the conclusion that overall significant increases in endogenous acetylcholine levels lead to decreases in the functional activity of the hippocampus and neocortex and that the mechanisms of cholinergic modulation of the theta and beta rhythms are significantly different. It is suggested that conditioned reflex switching, contextual learning, and dissociated sates of memory and consciousness are to a significant extent dependent on long-term changes in the oscillatory activity of the hippocampus and neocortex.