Summary and Conclusions
In the first part of this study, the arguments supporting the theory of the duality of sleep (slow sleep-paradoxical sleep) are set forth.
(1) Both tonic and phasic EEG or peripheral index of P.S. are totally different from EEG and behavioural slow sleep. The pontine origin of rapid eye movements and of the phasic ponto-geniculo-occipItal. activity occurring during P.S. is emphasized.
(2) Phylogenetic study shows that slow sleep may be observed in reptiles, birds and mammals. In contrast, P.S. is not found at all in the tortoise, and is of very short duration in birds (its ratio to the total sleep being only 0.2%). In mammals this ratio is about 6-30%).
(3) Ontogenetic studies in the kitten show that P.S. may appear immediately after wakefulness and constitutes 90% of total sleep during the first days. During maturation, the relative percentage of P.S. decreases to 30% while the percentage of slow sleep increases to 70% of the total sleep.
(4) The results of selective deprivation of P.S. in the adult animal are summarized. They show that after deprivation for more than 72 h, a maximum of 60% of P.S. is reached during recuperative sleep. This percentage is not exceeded even after 17 days of deprivation. On the other hand, during recuperation P.S. may be observed immediately after waking. After prolonged deprivation several days are required before the animal recovers the control level of P.S.
(5) Coagulation of the pons may suppress P.S. electively without producing any change in slow sleep.
(6) In chronic pontile animals, with hypothalamic islands, the rhombencephalic phase of sleep, showing all the pontine electrical and behavioural criteria of P.S. in the intact animal, can be completely identified with the latter. Its mean duration (6 min) is analogous to that of the intact animal while its duration per 24 h is somewhat less (10%). No behavioural or EEG index of slow sleep was observed in pontile animals.
All these results cannot be explained by a unitary theory of sleep. On the contrary, they allow us to differentiate P.S. from slow sleep in its structural bases and mechanisms.
The second part of the paper outlines some mechanisms of triggering P.S. in pontile animals.
It is possible to trigger reflex P.S. by proprioceptive or nociceptive stimulation in pontile animals, provided that the section is made caudally to the mesencephalic tegmentum. Various nervous deafferentations (afferents going through the spinal cord below C6, the vagus, buffer nerves) do not prevent P.S. from occurring in intact cats, and it does not therefore seem possible that P.S. is only triggered by reflex nervous pathways.
Ablation of the pituitary and hypothalamus does not suppress P.S. during the first 5 days of survival. A hormonal hypothalamo-pituitary mechanism is thus ruled out.
Deprivation of P.S. by electric shocks in pontile animals involves the reappearance, with increasing rapidity, of P.S., so that after a few hours P.S. can recommence several times per minute. This fact speaks for an active mechanism at the level of the pons.
The action of hypothermia on P.S. is considered and the resistance of this phenomenon to hypothermia shown.
The facilitatory effect of gamma-butyrolactone is emphasized. It was also found that P.S. is suppressed by hypo-osmolarity and facilitated by hyper-osmolarity of the blood.
All these results speak in favour of a self-regulating metabolic process, located in the pons, and the possibility of a neuroglial mechanism is considered.