Abstrakt: |
Cognitive processes are carried out during wakefulness by means of extensive interactions between cortical and subcortical areas. In psychiatric conditions, such as psychosis, these processes are altered. Interestingly, REM sleep where most dreams occurs, shares electrophysiological, pharmacological, and neurochemical features with psychosis. Because of this fact, REM sleep is considered a natural model of psychosis. Ketamine is a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist that at sub-anesthetic dose induces psychotomimetic-like effects in humans and animals, and is employed as a pharmacological model of psychosis. Oscillations in the gamma frequency band of the electroencephalogram (EEG), mainly at about 40 Hz, have been involved in cognitive functions. Hence, the present study was conducted to analyze the EEG low gamma (30–45 Hz) band power and coherence of the cat, in natural (REM sleep) and pharmacological (sub-anesthetic doses of ketamine) models of psychosis. These results were compared with the gamma activity during alert (AW) and quiet wakefulness (QW), as well as during non-REM (NREM) sleep. Five cats were chronically prepared for polysomnographic recordings, with electrodes in different cortical areas. Basal recordings were obtained and ketamine (5, 10, and 15 mg/kg, i.m.) was administrated. Gamma activity (power and coherence) was analyzed in the abovementioned conditions. Compared to wakefulness and NREM sleep, following ketamine administration gamma coherence decreased among all cortical regions studied; the same coherence profile was observed during REM sleep. On the contrary, gamma power was relatively high under ketamine, and similar to QW and REM sleep. We conclude that functional interactions between cortical areas in the gamma frequency band decrease in both experimental models of psychosis. This uncoupling of gamma frequency activity may be involved in the cognitive features shared by dreaming and psychosis. [ABSTRACT FROM AUTHOR] |