The Brain's Role In Regulating Rem Sleep

REM sleep is a unique phase of sleep in mammals and birds, characterised by random rapid movement of the eyes, low muscle tone throughout the body, and the propensity of the sleeper to dream vividly. The core body and brain temperatures increase during REM sleep, while skin temperature decreases.

REM sleep is physiologically different from the other phases of sleep, which are collectively referred to as non-REM sleep (NREM sleep, NREMS, synchronised sleep). The absence of visual and auditory stimulation (sensory deprivation) during REM sleep can cause hallucinations.

The electrical and chemical activity regulating REM sleep seems to originate in the brain stem, and is characterised by an abundance of the neurotransmitter acetylcholine, combined with a near-complete absence of monoamine neurotransmitters histamine, serotonin and norepinephrine.

REM sleep is controlled by the pons, which was demonstrated to be necessary and sufficient for the generation of REM sleep soon after its discovery in humans in 1953. However, researchers have since identified further neural populations in the hypothalamus, midbrain, and medulla that regulate REM sleep by either promoting or suppressing this brain state.

The pons is necessary and sufficient for the generation of REM sleep

The pons is a crucial region for the generation of REM sleep. Transection studies have determined that the pons is sufficient to generate much of the phenomenology of REM sleep.

The pons contains a complex variety of cells differing in their neurotransmitter, receptors and axonal projections. Unit recording techniques allow an analysis of the interplay between these cell groups and their targets to further refine our identification of REM sleep mechanisms.

The key brain structure for generating REM sleep is the pons and adjacent portions of the midbrain. These areas and the hypothalamus contain cells that are maximally active in REM sleep, called REM-on cells, and cells that are minimally active in REM sleep, called REM-off cells.

Subgroups of REM-on cells use the transmitter GABA, acetylcholine, glutamate, or glycine. Subgroups of REM-off cells use the transmitter norepinephrine, epinephrine, serotonin, histamine, and GABA.

Destruction of large regions within the midbrain and pons can prevent the occurrence of REM sleep. Damage to portions of the brainstem can cause abnormalities in certain aspects of REM sleep.

REM sleep is characterised by random rapid movement of the eyes, low muscle tone, and vivid dreams

REM sleep, or rapid eye movement sleep, is a unique phase of sleep in mammals (including humans) and birds. It is characterised by random rapid movement of the eyes, low muscle tone throughout the body, and the tendency of the sleeper to dream vividly.

During REM sleep, the eyes move rapidly behind closed eyelids, and the heart rate speeds up. The body experiences a temporary loss of muscle tone, which researchers hypothesise is a protective measure to stop the sleeper from acting out their dreams and injuring themselves. However, this hypothesis is now being questioned, as it has been discovered that dreams can occur during non-REM sleep, when the body is not paralysed.

REM sleep is the fourth of four stages of sleep. The first stage is light sleep, where the body has some muscle tone and breathing is regular. The second stage is also light sleep, but the heart rate and body temperature decrease, and the brain begins to show specific wave patterns. The third stage is deep sleep, where brain waves are at their slowest and the body physically repairs itself. The fourth stage is REM sleep, where brain activity is similar to when awake, and the body experiences a loss of muscle tone.

The first cycle of REM sleep occurs about 60-90 minutes after falling asleep, and each cycle takes 90-120 minutes to complete. As sleep continues, cycles shift towards a higher proportion of REM sleep. Most adults need about two hours of REM sleep each night.

REM sleep is important for memory consolidation, emotional processing, brain development, and dreaming. It is also associated with an increase in brain temperature and a decrease in skin temperature.

REM sleep is physiologically different from other phases of sleep

REM sleep is physiologically distinct from other phases of sleep, also known as non-REM sleep. During REM sleep, the body and brain temperatures increase, while the skin temperature decreases. The brain exhibits high energy use, with brain activity resembling that of a waking state. This includes fast, low-amplitude, desynchronized neural oscillation (brainwaves) and heightened activity in areas of the brain associated with memory, emotion, fear, and sex. REM sleep is also characterised by an abundance of the neurotransmitter acetylcholine, combined with an absence of monoamine neurotransmitters. The body experiences muscle atonia, with a loss of muscle tone, and the eyes exhibit rapid movement.

REM sleep is preceded by non-REM sleep and the two states alternate within a sleep cycle, which lasts around 90 minutes in adult humans. Non-REM sleep is further divided into three stages, with each stage being progressively deeper than the last. During non-REM sleep, the body repairs tissues, builds bone and muscle, and strengthens the immune system. In the deepest stage of non-REM sleep, the body temperature drops, breathing slows, and blood pressure decreases.

The core circuitry generating REM sleep is localised in the brainstem

REM-on neurons are primarily cholinergic and are located in the subcoeruleus area in cats or the sublaterodorsal nucleus (SLD) in rodents. These neurons induce muscle atonia during REM sleep.

REM-off neurons are located in the ventrolateral periaqueductal gray matter (vlPAG) and dorsal raphe (DR) and locus coeruleus (LC). These neurons suppress REM sleep.

The vlPAG is a key node in the REM sleep circuitry, as it is both sufficient and necessary for gating REM sleep.

The mutual inhibition between REM-on and REM-off neurons is thought to generate the repeated transitions between NREM and REM sleep.

REM sleep is under homeostatic control

REM sleep is regulated by the brainstem, specifically the pons, which was demonstrated to be necessary and sufficient for the generation of REM sleep. REM sleep is also regulated by the hypothalamus, midbrain, and medulla. REM sleep is controlled by the interaction of REM sleep-promoting (REM-on) and REM sleep-suppressing (REM-off) neurons. The 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.

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