The transition from slow-wave sleep to paradoxical sleep: evolving facts and concepts of the neurophysiological processes underlying the intermediate stage of sleep.

Paradoxical sleep in rats, cats and mice is usually preceded and sometimes followed by a short-lasting (a few seconds) electroencephalogram (EEG) stage characterized by high-amplitude spindles in the anterior cortex and low-frequency theta rhythm in the dorsal hippocampus. The former is an index of advanced slow-wave sleep; the latter is an index of limbic activation since it occurs during active waking and paradoxical sleep. Barbiturates and benzodiazepines extend this intermediate stage at the expense of paradoxical sleep while concomitantly barbiturates suppress the pontine reticular activation characteristic of this sleep stage. During the intermediate stage, thalamocortical responsiveness and thalamic transmission level, which are controlled by brain stem activating influences, are the lowest of all sleep-waking stages. The unusual EEG pattern of this stage is otherwise only observed in the acute intercollicular-transected preparation. Therefore, forebrain structures may be functionally briefly disconnected from the brain-stem during this short-lasting stage, which could possibly account for the mental content of a similar sleep period in humans. In spite of strong evidence in favour of this forebrain deafferentiation hypothesis, other data indicate that the IS is in some way linked either to slow-wave sleep or to paradoxical sleep.