PT  - JOURNAL ARTICLE
AU  - Stata Norton
AU  - Robert E. Jewett
TI  - EFFECT OF DRUGS ON SPONTANEOUS SLOW POTENTIAL OSCILLATIONS OF THE CEREBRAL CORTEX
DP  - 1965 Sep 01
TA  - Journal of Pharmacology and Experimental Therapeutics
PG  - 301--310
VI  - 149
IP  - 3
4099  - http://jpet.aspetjournals.org/content/149/3/301.short
4100  - http://jpet.aspetjournals.org/content/149/3/301.full
SO  - J Pharmacol Exp Ther1965 Sep 01; 149
AB  - Using nonpolarizable electrodes and d.e. amplifiers, rhythmic oscillations of the steady potentials can be recorded from the cortex of conscious, unrestrained cats. These waves represent a continuous spectrum with the electro-encephalogram. Three main frequency groups are distinguishable: 8-12 cpm, 3-5 cpm and 0.5.5-1.5 cpm. Voltages of these waves range from 1100 to 600 µV. During activated sleep (low voltage, desynchronized EEG) there is a negative shift of 400-1000 µV. Except for the 8-12 cpm waves, which were not quantified, all slow waves, including periodic shifts with activated sleep, were blocked by amphetamine and chlorpromazine but not by sedative doses of BW 58-271 or thiopental. Motor behavior in response to an environmental stimulus (handling the cats) was not depressed by amphetamine but was markedly reduced by chlorpromazine, BW 58-271 or thiopental. After amphetamine the EEG showed a continuous desynchronized, low voltage pattern when the cats were undisturbed, while following chlorpromazine the EEG stayed in a synchronized light sleep pattern. Evidence that the origin of the cortical slow waves and shifts during sleep patterns may be either limbic or reticular is discussed. The clear difference between the effects of chlorpromazine and anesthetic agents tends to support the limbic control of activated sleep postulated by Jouvet and Jouvet (1963). The Williams & Wilkins Comapny