Approximately 20% of Charles River rats which were chronically implanted with brain electrodes for EEG recordings exhibited within half a year of the implantation spontaneous, paroxysmally occurring, steep EEG potentials of high amplitude (spikes and waves) whilst falling asleep. These EEG paroxysms were dose dependently antagonized by the ‘petit mal drugs dipropylacetate, ethosuximide and trimethadione as well as by the anticonvulsant drugs diazepam and nitrazepam. The neuroleptics chlorpromazine, haloperidol and thioridazine prolonged the EEG paroxysms. The α1-adrenoceptor antagonist prazosin and the α2-adrenoceptor agonists guanfacine and clonidine prolonged, whereas the α2-adrenoceptor antagonist yohimbine shortened, the EEG paroxysms. The effect of guanfacine was antagonized by yohimbine. The convulsant drugs bicuculhne, 3-mercaptopropionic acid and pentetrazol had only a slight influence on the EEG paroxysms. The results are discussed with respect to the anti- and proconvulsant and convulsant activity of psychotropic drugs and their underlying mechanisms of action, particularly with regard to their interaction with central α-adrenergic mechanisms.