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Neurobiology of Dreams: Neural Mechanisms


Fig.1. Monkey brain depicting the brain stem reticular formation. In pink: Part 
of the reticular formation of the brainstem
whose stimulation induces arousal. Sensory pathways ascending from spinal and brain stem levels to the somesthetic receiving area of cortex. The reticular formation contains projections which influence the hypothalamus and, at the level of thalamus, diverge to distribute impulses diffusely throughout all areas of cortex. (Modified of Levingston, 1967). 

In a higher animals and human beings, the switching of states of awake and sleep happens due to existence of special nervous structures.

Rem sleep, the "dream sleep", is quite different from non-REM sleep. The cortex in this state is as active during REM sleep as it is during waking. The cortex is not necessary for the production of REM, but it certainly is required for dream's elaboration.

The brain activity during REM, begins in the pons, a structure in the brainstem and neighboring midbrain regions. The pons sends signals to the thalamus and to the cerebral cortex, which is responsible for most thought processes. It also sends signals to turn off motor neurons in the spinal cord, causing a temporary paralysis that prevents movement. 

Some researchers have used positron emission tomography (PET) to study the brain state associated with REM sleep in humans (Maquet et al, 1996 - da Internet). The results show that regional cerebral blood flow is positively correlated with REM sleep in:

Given the role of the amygdaloid complexes in the acquisition of emotionally influenced memories, the pattern of activation in the amygdala and the cortical areas provides a biological basis for the processing of some types of memory during REM sleep.

Biochemical Mechanisms of REM sleep

Scientists found that sleep phases are closely related to the activity of certain groups of nerve cells releasing brain chemicals that relay information from one neuron to another. Research on these specialized cell groups is helping scientists to devise specific drug treatments for sleep disorders.

The brain has several colletions of neurons, each using a particular neurotransmitter and making difuse connections. These cells perform regulatory functions influencing a large number of postsynaptic neurons in spinal cord, thalamus, cerebral cortex, and so on, so they become more or less exitable. Different systems (such as noradrenergic, serotonergic and cholinergic) appear to be essential for aspects of metabolic state, motivation, motor control, memory, etc.

In his article, Hobson (bear, 1996) wrote that the most surprising observation that he and his coworkers made was that both the noradrenergic locus coeruleus and the serotonergic raphe neurons "turn off" in REM sleep (table 1). This finding was a surprise because every one had predicted the opposite. For him, It was clear that these two aminergic systems supported waking and not sleep, as had been theorized. REM sleep could be triggered by cholinergic stimulation of the reticular formation. It is probably the action of ACh during REM sleep that causes the thalamus and the cortex to behave so much like they do in the wake state.
(Locus coeruleus)
(Raphe nuclei)

(cortex, septal nucleus,

Table 1. Differential activity of specific neurochemical subsystems of the brain stem in waking and REM sleep. The firing rates of the two major systems of the upper brain stem, the locus coeruleus and the Raphe nuclei , "turn off" the REM sleep, that is, they decrease to almost nothing with the onset of REM. However, there is a current sharp increase in the firing rates of ACh-containing neurons in the pons, and some evidence suggests that cholinergic neurons induce REM sleep. It is probably the action of ACh during REM sleep that causes the thalamus and cortex to behave so much like they do in waking state (Bear, 474). REM periods are terminated when norepinephrine and ACh-containing neurons begin firing again.

Why Don't We Act Out During REM Sleep? (next page)

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Author: Silvia Helena Cardoso, PhD. Psychobiologist, master and doctor in Sciences by the University of São Paulo and post doctoral fellowship by the University of California, Los Angeles. Invited Professor and Associate Researcher of the Center for Biomedical Inofrmatics, State University of Campinas (Unicamp), Brazil.Email:

Translation: SIlvia Helena Cardoso

Center for Biomedical Informatics
State University of Campinas, Brazil

Silvia Helena Cardoso, PhD

Copyright 1997 State University of Campinas