Neurophysiology of the States of Sleep
Michel Jouvet
Physiological Reviews 47 (2) pp : 117-177 (1967)


Definitions and Abbreviations

State of Sleep Characterized by Slow Cortical Activity Slow Sleep

Behavioral aspect

Electrophysiological aspect

Structures and mechanisms responsible for slow sleep

State of Sleep Characterized by Fast Cortical Activity-Paradoxical Sleep

Behavioral aspects

Electrophysiological aspects

Structures and mechanisms responsible for paradoxical sleep

A synthesis of paradoxical sleep mechanisms

Relationship with oneiric activity in man

Phylogenesis of the States of Sleep

Ontogenesis of the States of Sleep

Relationship Between Slow Sleep and Paradoxical Sleep Unicity or Duality of Sleep Mechanisms

A Possible Monoaminergic Theory of Sleep

Figure 1

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III. State of sleep characterized by fast cortical activity paradoxical sleep

D. A Synthesis of Paradoxical Sleep Mechanisms

Even though it seems perhaps premature, we may try to distinguish between the facts and the hypotheses concerning the two major problems about PS

1) which are the intrinsic mechanisms, and

2) which are the triggering mechanisms?

1) Numerous data suggest that PS is accompanied by an increase in neuronal activity an increase in unitary cortical and reticular activity (140, 224), background level of pyramidal activity (20), and cortical excitability (estimated from evoked responses). However, it still remains to be proved whether this increase of activity is due to the mere intervention of the ARAS (at a level identical with or superior to that of intense wakefulness) or if it is a different mechanism (as might be thought from the disorganization of cortical unit activity). Then it should be assumed that PS is the manifestation of an intense disinhibitory state (superior to that of slow sleep) of the cortical and reticular neurons (but that during waking an inhibitory control would be exerted only on the former) (142).

However, PS does not seem to be the expression of the same neuronal processes (even at cortical level) underlying slow sleep (142). The data of cerebral impedance (50), cerebral temperature (266, 367), cerebral blood flow (261), and cortical steady potential (442) are, on the contrary, in favor of the appearance of a new state that is in accordance with the neuropharmacological data. The problem of ascending structures, ascending from the pons and responsible for fast cortical activity and for occipItal. and geniculate monophasic spikes, has not yet been totally solved. The persistence of cortical activation after important lesions of the specific or nonspecific formations of the brain stem makes a neurohumoral mechanism very likely.

Whatever the efferent results of this tonic and phasic increase in neuronal activity may be, a tonically active, very powerful mechanism triggers from the pons the inhibitory reticular formation that blocks, at a pre- or postsynaptic level, the discharges of spinal motoneurons (except phasic discharges and ocular movements). This intervention of the inhibitory RF might account for some of the contradictory aspects concerning the arousal threshold. To induce behavioral arousal, the electrical stimulation of the ARAS must indeed run the blockade exerted by the inhibitory RF at the motoneuron level, when the ARAS may itself be in its maximum state of excitability. Then PS might be compared to a hyperwakefulness state in a preparation under curare (but blocking of the efferents would be at the spinal and not the neuromuscular level).

2) On the one hand, PS represents the expression of an active process; as a matter of fact, it may be triggered by high-frequency stimulations of the brain stem and abolished by local coagulation at the pontine level. Moreover, this whole mechanism is resistant to hypothermia and the PGO phasic activity is somewhat resistant to Nembutal narcosis.

The triggering cause of PS does not appear to be necessarily situated at the pontine level after pontine RF coagulations preventing PS, periodical behavioral disturbances (hallucinatory-like state), perhaps expressing the reaction of the nervous system to the cause (humoral or neurohumoral) that would normally trigger PS, may be observed. Pontine triggering structures appear as effectors with ascending or descending action. The existence of a refractory phase, during which it is impossible to trigger PS by stimulation, compels us to admit that there is a triggering threshold in the intrinsic cause of PS, although the intrinsic periodicity of PS (and its limited duration even after long deprivations) supports the theory of a self-regulating process.

Though numerous factors, hormonal (in the rabbit), humoral (hyperosmolarity), or pharmacological (short-chain fatty acids), may facilitate PS, the triggering factor is still unknown, nor are the triggering mechanisms of the periodical rhythm of PS in pontine animals. It cannot be ascribed to a hypothalamopituitary factor nor to the action of a nervous peripheral mechanism. Finally, the presence of numerous noradrenergic neurons in the dorsal part of the mediolateral pontine tegmentum associated with the dramatic effect of reserpine suggests that PS could be the expression of some mechanism involving cerebral monoamines. We do not know its subjective aspect in animals, of course, but numerous data strongly sug gest that oneiric activity occurs during PS in man.

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