A Study of the Neurophysiological Mechanisms of Dreaming
M. Jouvet and D. Jouvet Electroenceph. Clin. Neurophysiol. 1963 Suppl. 24
TABLE OF CONTENTS

Introduction

Methods
Part 1

I. Two EEG patterns of physiological sleep in intact cats

II. The neural structures responsible for RPS

III. Structures responsible for somato-vegetative phenomena

IV. Mechanisms of the Rhombencephalic Phase of Sleep

V. Ontogenesis of the RPS
Part 2

A. Normal subjects

B. Patients with brain lesions

Discussion

Summary
Figures

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Part 1 : Experimental results obtained on cats

The rhombencephalic phase of sleep Results

IV. Mechanisms of the Rhombencephalic Phase of Sleep

This is an active phenomenon as it is possible to trigger off the appearance of RPS by stimulating the pontile RF of the intact animal, provided that stimulation occurs during SPS ( Fig. 11).

In mesencephalic cats, stimulation of this same zone is also capable of triggering periods of "Rhombencephalic Sleep". Phases of 15 min duration have thus been obtained after stimulations lasting 1-2 sec. After the animal has spontaneously awakened, a refractory period is observed, during which an identical stimulus determines a hypertonic phase accompanied by agitation. Therefore, it is never possible to trigger several periods of rhombencephalic sleep successively. An interval of 15-20 min must be allowed to elapse before a new stimulation can produce a new phase of sleep. In some animals, sleep has been obtained by summation of stimuli of long duration (10-20 sec) and in some cases a latent period of 30-60 sec was observed between the end of the stimulation and the beginning of sleep.

Atropine (0.2-0.3 mg/kg) considerably reduces the duration of RPS or even stops it from appearing, particularly in mesencephalic animals. On the other hand, the injection of cholinergic drugs (eserine) produces longer RPS although their frequency is not increased.

These facts are difficult to explain as a whole through purely neuronal mechanisms. They lead us to hypothesize the existence of a neurohumoral mechanism which would "discharge" periodically during behavioral sleep but which could not be brought into play until a sufficient "stock" of neurohormones has been accumulated.

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