Abstract
Chlorpromazine causes slow wave activity to become dominant in the spontaneous EEG and depresses the activating response evoked by auditory and sciatic nerve stimulation, direct stimulation of the bulboreticular formation, and epinephrine.
Activation induced by direct electrical stimulation of the reticular formation seems to be more easily depressed by chlorpromazine when the rostral portion of the brain stem is stimulated than by stimulation of more caudal locations.
Cortical potentials evoked by a variety of stimuli appear diffusely over the cortex and with larger amplitude following chlorpromazine than before. Therefore, since these potentials must be mediated by an extralemniscal pathway, it is unlikely that chlorpromazine acts by blocking sensory transmission to this system.
All phenothiazine derivatives investigated produced a slowing of the EEG, a depression of its activation and an enhancement of single potentials evoked diffusely over the cerebral cortex.
Those compounds, chlorpromazine and KS 24, which have been found to be most effective in agitated psychosis, have a long duration of action.
Footnotes
- Received October 12, 1957.
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