Rapid eye movement (REM) sleep

Neurophysiology

Cortical activity

There are regional differences in cortical activity in REM sleep. The dorsolateral prefrontal cortex is particularly inactive. Unlike NREM sleep in which the thalamic 'gate' partially disconnects the cortex from the brainstem, the cortex still reacts to sensory information but in a different way than during wakefulness. The exception is that there is little activity in the spinoreticular tract which mediates pain, and painful sensations are very unusual in dreams.

There is evidence for interhemispheric disconnection compared to wakefulness, but similar to that which is seen after sectioning of the corpus callosum.

Transcranial magnetic stimulation has revealed this disconnection particularly in the frontal and central areas of the cortex compared with the parietal and occipital regions _[8]. It may be responsible for some of the lack of insight during dreams, time distortion and failure of some subjects to report dreams.

Muscle atonia
The pontine reticular formation ventral to the locus coeruleus (peri-locus coeruleus), including the LDT/PPT nuclei, projects to the nucleus magno-cellularis and nucleus paramedianus in the medial medullary reticular formation via the lateral tegmento-reticular tract (Fig. 2.2). Glutamate, which acts on receptors of the NMDA type, and acetylcholine are released and excite neurones in these nuclei. They project via the ventrolateral reticulospinal tract to the alpha motor neurones. The medial medullary centres are also activated by the locus coeruleus and the red nucleus which thereby reduce muscle tone. The motor neurones in the cranial nerve nuclei and spinal cord are inhibited by release of glycine, and this leads to the intense muscle atonia which is characteristic of REM sleep.

The continuous activity of the cerebral cortex is transmitted to the basal ganglia which remain active in REM sleep, but the complex behaviour patterns that they formulate are not enacted because of the intense inhibition of skeletal muscle tone.

Phasic activities
Many of the manifestations of REM sleep occur irregularly and apparently spontaneously due to intrinsic activity of the brainstem mechanisms responsible for REM sleep. These phasic activities include:

Muscle atonia
The pontine reticular formation ventral to the locus coeruleus (peri-locus coeruleus), including the LDT/PPT nuclei, projects to the nucleus magno-cellularis and nucleus paramedianus in the medial medullary reticular formation via the lateral tegmento-reticular tract (). Glutamate, which acts on receptors of the NMDA type, and acetylcholine are released and excite neurones in these nuclei. They project via the ventrolateral reticulospinal tract to the alpha motor neurones. The medial medullary centres are also activated by the locus coeruleus and the red nucleus which thereby reduce muscle tone. The motor neurones in the cranial nerve nuclei and spinal cord are inhibited by release of glycine, and this leads to the intense muscle atonia which is characteristic of REM sleep.