Electrocortical Desynchronization Research Articles

BEHAVIORAL AND ELECTROENCEPHALOGRAPHIC AROUSAL TO CONTRASTING NOVEL STIMULATION.

Three-second interruptions of continuous auditory stimulation, as well as 3-second periods of stimulation from the same sound source, were effective in producing behavioral arousal and electrocortical desynchronization in sleeping cats. Thus, stimulus offset as well as onset may serve an arousal function. Some differences in behavioral response and electrocortical desynchronization latency were noted.

Ocular phenomena in the two stages of sleep in the cat

The pupil is wider and the nictitating membrane is more retracted in the stage of sleep characterized by a low voltage electrocorticogram than in sleep with slow waves and spindles. The infrapalpebral events suggest an increased sympathetic activity, probably humoral in nature, which may help account for some of the variations in autonomic neuroeffector systems and the persistent electrocortical desynchronization typical of this stage of sleep.

Demonstration of anti-depressant or stimulant properties of imipramine in experimental animals.

IMIPRAMINE (I) is a drug that is related chemically to the major tranquillizers of the phenothiazine group such as chlorpromazine (II). As distinct from chlorpromazine, however, imipramine is claimed to be of considerable value in the treatment of depression, particularly of the endogenous type1–3. Pharmacologically, imipramine has many of the properties of chlorpromazine although it is quantitatively less potent. Thus in the mouse, imipramine, like chlorpromazine, reduces motor activity, prolongs hexobarbitone sleeping time, and causes a fall in rectal temperature4,5. Both imipramine and suitable doses of chlorpromazine counteract the hypothermia, ptosis, bradycardia, and diarrhœa caused by reserpine administration in rats6, and both drugs produce sedation in the cat and dog4. In the curarized cat, both drugs block the electrocortical desynchronization caused by electrical stimulation of the mesencephalic reticular formation4, although it has been suggested7 that this action of imipramine is due to atropine-like properties rather than to chlorpromazine-like sedation. Slight qualitative differences have been observed between chlorpromazine and imipramine in their action on the electrical activity recorded from certain sub-cortical areas in the rabbit. The resemblance between the pharmacological actions of these two drugs has led to the view6 that the differences between the pharmacological effects of chlorpromazine and imipramine are, at present, only quantitative, rather than qualitative. Furthermore, unlike other drugs, such as iproniazid and nialamide, used at present in the treatment of depressive illnesses, imipramine is not an inhibitor of mono-amine oxidase9. There appeared, therefore, to be no pharmacological basis for its important clinical anti-depressant properties.