By Olga Petre-Quadens
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NEURAL MECHANISMS OF THE SLEEP-WAKING CYCLE 21 the first postoperative week, when EEG synchronization was complete, confirming the original findings of Bremer (1935, 1937, 1938c). As lapses of EEG desynchronization began to appear, the myosis became less marked. The chronic cerveau isole cats were followed for quite long periods of time, 15—72 days. Eventually, cycles of desynchronization—synchronization reappeared. They were accompanied by corresponding changes in the pupillary diameter, similar in sign to those observed during sleep and wakefulness in blinded cats by Berlucchi et al.
The reappearence of the ability to maintain wakefulness for some time is related to the progress of chronicity, and humoral transmission from the brain stem can hardly account quantitatively for the phenomenon; also there is so far no convincing proof of the existence of denervation hypersensitivity in the isolated cerebrum. Thus the ability to maintain a waking state, and to alternate between sleep and wakefulness, arises within the isolated cerebrum. The statement that humoral mediation cannot account quantitatively for the existence of a sleep—waking cycle in the isolated cerebrum does not imply that the hypothesis of humoral connections is altogether disproved.
Parietal (P) and occipital (O) left (L) and right (R) leads. B. EEG desynchronization, 5 min after intracarotid injection of 10 mg of dopa. C. Synchronized pattern 2 hr after B (and 5 min after intravenous injection of 10 mg of dopa). The effect of the intravenous injection (slight increase of the interspindle lulls) is much smaller than that of the intracarotid injection. LFrom Mantegazzini and Glässer, i960] should be transformed, locally, into the noradrenaline mediator. Concerning hypothesis (1), two objections may be raised: (a) Where do the synthesizing enzymes come from, when axons are n o longer connected with the soma?