What Activates Your Brain During Rem Sleep?

REM sleep is a distinct, homeostatically controlled brain state characterised by an activated electroencephalogram (EEG) in combination with paralysis of skeletal muscles and is associated with vivid dreaming. The core circuitry generating REM sleep is localised in the brainstem, but populations of neurons powerfully regulating REM sleep by either promoting or suppressing this brain state have been found throughout the medulla, pons, midbrain, and hypothalamus.

Brain Regions Involved in REM Sleep

The brain regions involved in REM sleep are located in the brainstem, forebrain, and hypothalamus. The core of the REM-generating circuit is located at the mesopontine junction, medial to the trigeminal motor nucleus and ventral to the locus coeruleus. The subcoeruleus nucleus (SubC) is composed of REM-active neurons and is thought to regulate REM sleep and its defining features such as muscle paralysis and cortical activation. The majority of REM-active SubC cells are glutamatergic, but GABA SubC cells have also been implicated in REM sleep control.

REM sleep is also characterised by a constellation of events, including low-amplitude synchronization of fast oscillations in the cortical EEG, very low muscle tone in the EMG, and singlets and clusters of REMs in the EOG. REM sleep is associated with an intense neuronal activity, similar to waking levels.

REM sleep is also associated with the presence of pontine–geniculate–occipital (PGO) waves as well as hippocampal theta EEG activity. Compared to NREM sleep, REM sleep is considered the sleep state with the highest physiological arousal. Respiration, heart rate, and brain glucose utilization are more variable and activity can be as high as that observed during wakefulness. However, skeletal muscle activity is actively inhibited during REM sleep.

REM sleep is also associated with a high activity in the brainstem and thalamic nuclei as well as in limbic and paralimbic areas: the amygdala, the hippocampal formation, and the anterior cingulate, orbitofrontal, and insular cortices. Temporal and occipital cortices as well as motor and premotor areas are also shown to be very active during human REM sleep.

Neurotransmitters and Meural Activation

Neuronal activity during REM sleep has been proposed to associate with various brain functions, including memory consolidation. REM sleep is characterised by distinct global cortical activity and is distinct from wakefulness and NREM sleep. The REM sleep core is located in the brainstem and is composed of REM-active neurons. REM-active neurons in the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus trigger REM sleep muscle atonia by activating neurons in the ventral medial medulla (VMM), which causes the release of GABA and glycine onto skeletal motoneurons. REM sleep timing is controlled by activity of GABAergic neurons in the ventrolateral periaqueductal gray and dorsal paragigantocellular reticular nucleus as well as melanin-concentrating hormone neurons in the hypothalamus and cholinergic cells in the laterodorsal and pedunculo-pontine tegmentum in the brainstem. REM sleep is also controlled by a dispersed network of different transmitter systems, including the dopaminergic system. The REM sleep core is thought to be a glutamatergic mechanism, with the majority of REM-active SubC cells being glutamatergic. However, GABA SubC cells have also been implicated in REM sleep control. REM sleep is also associated with an intense neuronal activity, similar to wakefulness. REM sleep is generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus.

Role of Meural Activation in Dreaming

The role of meural activation in dreaming is not well understood. However, REM sleep is characterised by muscle paralysis, rapid eye movements, and vivid dreaming. REM sleep is thought to be generated and maintained by the interaction of a variety of neurotransmitter systems in the brainstem, forebrain, and hypothalamus. The core of the REM-generating circuit is located in the mesopontine junction, medial to the trigeminal motor nucleus and ventral to the locus coeruleus. Glutamatergic neurons in the subcoeruleus nucleus (SubC) or sublaterodorsal nucleus trigger REM sleep muscle atonia by activating neurons in the ventral medial medulla, which causes release of GABA and glycine onto skeletal motoneurons. REM sleep is also associated with an intense neuronal activity, similar to wakefulness. REM sleep is also associated with a high activation of the occipital cortex during REM sleep, which is consistent with a human EEG study, which shows that the 'dreaming' experience is tightly correlated with activation of the occipital "hot zone".

REM Sleep Behaviour Disorder

The person with RBD may be awakened or wake spontaneously during the attack and vividly recall the dream that corresponds to the physical activity. RBD is usually seen in middle-aged to elderly people and more often in men. The exact cause of RBD is unknown, but it may happen alongside degenerative neurological conditions such as Parkinson's disease, multisystem atrophy (also known as Shy-Drager syndrome), and diffuse Lewy body dementia.

The primary treatment goal of RBD is to reduce the risk of injury to the patient and bed partners. This may involve mitigating fall risk by lowering the bed closer to the floor, safe-guarding any firearms, knives, and other weapons, and placing patients in restraining clothes or sleeping bags.

Impact of Sleep Deprivation on REM Sleep

Sleep deprivation can have a significant impact on REM sleep. The amount of REM sleep an individual experiences is directly related to the amount of sleep deprivation they have experienced. Studies have shown that shorter periods of sleep deprivation, up to 6 hours, result in increased non-REM sleep. However, longer periods of deprivation, ranging from 12 to 24 hours, lead to an increase in both non-REM and REM sleep. When sleep deprivation is extended to approximately 96 hours, individuals exhibit a marked increase in REM sleep and experience REM rebound.

REM rebound is a compensatory response in which an individual experiences increased REM sleep temporarily. It is characterized by vivid dreams, accompanied by REMs, paralysis of skeletal muscles, and EEG patterns indicating an activated cerebral cortex. This phenomenon is the result of neurophysiological and hormonal processes that are essential for maintaining normal sleep patterns and overall homeostasis.

Several factors can contribute to REM rebound, including sleep deprivation, withdrawal from REM-suppressing medications, substance withdrawal, depression, and the initiation of continuous positive airway pressure (CPAP) therapy. Sleep deprivation, in particular, can negatively impact both physical and mental well-being, increasing the risk of various health conditions such as obesity, metabolic disorders, hypertension, and coronary artery disease. It can also lead to mood changes, irritability, and issues with cognition and problem-solving.

The impact of sleep deprivation on REM sleep is not limited to humans. Studies have shown that horses, for example, require specific conditions, such as lying down, to enter REM sleep safely. If they are unable or unwilling to lie down, they may experience a sudden loss of muscle tone and an increased risk of dangerous falls.

Frequently asked questions