Rapid eye movement sleep resemblance to waking life), and incorporation of instinctual themes. Sometimes they include elements of the dreamer's recent experience taken directly from episodic memory. By one estimate, 80% of dreams occur during REM. Hobson and McCarley proposed that the PGO waves characteristic of “phasic” REM might supply the visual cortex and forebrain with electrical excitement which amplifies the hallucinatory aspects of dreaming. However, people woken up during sleep do not report significantly more bizarre dreams during phasic REMS, compared to tonic REMS. Another possible relationship between the two phenomena could be that the higher threshold for sensory interruption during REM sleep
Rapid eye movement sleep brain stem. REM-on neurons are primarily cholinergic (i.e., involve acetylcholine); REM-off neurons activate serotonin and noradrenaline, which among other functions suppress the REM-on neurons. McCarley and Hobson suggested that the REM-on neurons actually stimulate REM-off neurons, thereby serving as the mechanism for the cycling between REM and non-REM sleep. They used Lotka–Volterra equations to describe this cyclical inverse relationship. Kayuza Sakai and Michel Jouvet advanced a similar model in 1981. Whereas acetylcholine manifests in the cortex equally during wakefulness and REM, it appears in higher concentrations in the brain stem during REM. The withdrawal of orexin and GABA may cause