Reflective waking mentation is supported by cortical activating and inhibitory processes. The thought-like mental content of slow wave sleep appears with lower levels of both kinds of influence. During REM sleep, the equation: activation + disinhibition + dopamine may explain the often psychotic-like mode of psychological functioning. [Hobson et al.; Nielsen; Revonsuo; Solms; Vertes & Eastman].

The descriptive “null” hypothesis is strengthened by the fact that during dreaming sleep stage, the primary visual cortex is deactivated as compared with other sleep stages.

During the paradoxical dreaming sleep stage, characterized by hallucinations and delusions, as in schizophrenia, the increased subcortical release of dopamine, the presynaptic inhibition of thalamic relay nuclei, and serotonergic disinhibition are in accordance with the model for the mechanism of hallucination-induction.

There are strong resemblances between the neurobiological characteristics of hallucinations occurring in the particular case of schizophrenia and the hallucinatory activity observed during the rapid-eye-movement (dreaming) sleep stage: the same prefrontal dorsolateral deactivation; forebrain disconnectivity and disinhibition; sensory deprivation; and acetylcholine, monoamine, and glutamate modifications.