The EEG and behavioral effects of threshold doses of harmaline (2–3 mg/kg) were studied in 4 chronically implanted freely moving intact cats and 5 chronic animals with complete mesencephalic transection. Further analysis of the EEG events was performed in 6 Flaxedil immobilized cats. Behaviorally, the drug induced intense motor activation, tonic postural and gait abnormalities, tremor, abnormal facial expression, crying and neuro-vegetative phenomena (mydriasis, salivation, deglutition, tachypnea, bradycardia) in both intact and physiologically decerebrate cats plus exploratory behavior in intact animals. The duration of these behavioral effects was two hours, after which the cats remained neurologically depressed. Paradoxical sleep was suppressed for about 7 hours.
Electrocortically, the drug induced intermittent or continous hypersynchrony which was most predominent over visual areas. In intact cats there was a short desynchronization immediately after the injection and in the “cerveau isolé” the drug induced a “synchronization period”. Subcortical rhythmic bursts of 10 to 15 c/sec were recorded from the pontine and mesencephalic reticular formation in all cases; these were shown to be independent of descending influences and nonmuscular in origin. The EEG recorded from the lateral geniculate body also exhibited slow (1.5–3 c/sec), high voltage (200 μV) activity.
The electrocortical synchronization as well as the paradoxical sleep suppressor effects are discussed in the light of the MAO inhibiting action of harmaline. The tremorogenic effect is attributed to lower brain stem motor mechanisms and considered to be related to the pontine reticular EEG events. The fact that many of the actions of this hallucinogen can be accounted for without the necessary participation of rostral brain structures is particularly stressed.