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

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VI. Relationship between slow sleep and paradoxical sleep or duality of sleep mechanisms

Reciprocal interrelations between slow sleep and PS are obvious PS only occurs in normal subjects (cat or man) after a slow sleep phase lasting a variable period, and that is why the theory of the unicity of sleep was set forth. According to this theory (197), an ascending and descending hypnogenic process would first affect the ARAS at the limbic midbrain area level (and so would account for the slow activity of slow sleep) and then would progressively invade, upward, the thalamic synchronizing structures (which would account for the disappearance of the recruiting response) and would thus provoke a fast cortical activity through inhibition of the thalamic synchronizing structures. However, the absence of any relationship between the duration of the previous slow sleep period and that of PS, and the persistence of a fast cortical activity after destruction of the thalamus, defeats any attempt to define the hypothetical mechanisms responsible for the invading of "inhibition" in the brain stem.

On the contrary, numerous results support a relative autonomy of the two states of sleep. It is possible to achieve elective suppression of PS by a pontine lesion without abolishing slow sleep, although there is usually only PS in pontine animals (in which it is not possible to observe behavioral or EEG phases of slow sleep), thus demonstrating duality of the structures in action. To this structural duality we may add some arguments in favor of some duality of mechanisms. A unitary theory of sleep necessarily implicates a preceding slow (light) sleep on PS, which is considered a phase of deep sleep According to this hypothesis, there must be some parallelism between the two states of sleep during their phylo- and ontogenetic evolution. Now neither ontogenetic nor phylogenetic data support such an idea. If slow sleep exists in all vertebrates (observed by polygraphic methods from the tortoise to man) PS, on the contrary, does not appear to be connected with the appearance of slow sleep during phylogenetic development. The lack of PS in chelonians and its very rudimentary aspect in birds contrast with its being relatively common and important in mammals. Though the number of animal species studied so far is still too small to draw permanent conclusions, it seems likely that PS occurs from the stage of birds upward during evolution. So we may suppose a new function to appear, not necessarily bound to slow sleep, since it is lacking in reptiles.

The data of ontogenesis also allow us to differentiate the development of the two states of sleep. At birth PS is relatively important and is totally independent of the slow sleep state. So, in newborn mammals, slow sleep is not necessary for the occurrence of PS. Consequently, we must assume the mechanism responsible for PS is pre-established at birth, whereas slow sleep is still little developed and seems to be governed by mechanisms acquired during postnatal maturation.

If, in the adult, the differentiation of behavioral sleep into two states is possible by means of the polygraph, the usual precedence of slow sleep over PS would allow us to assume that slow sleep is necessary for the appearance of PS. However, the selective deprivation technique enables us to dissociate them, since PS may be ob served immediately after wakefulness during recovery. This has also been noticed in adult man during narcoleptic or cataleptic attacks (368).

Slow sleep and PS appear, then, to be the manifestation of two processes, relatively opposite in their structures and mechanisms; thus it would be better to refer to different states rather than phases of sleep. Behavioral sleep in the adult mammal does not seem to develop according to a cycle, from light to deep sleep, but seems to include two states of activity, qualitatively different, of the nervous system. It is possible that these two states of activity are induced by different groups of monoaminergic neurons, as suggested in a possible monoaminergic theory of sleep, which is summarized next.

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