Brain Activity During Rem Sleep: Neural Messages Blocked

Non-rapid eye movement (NREM) sleep is an essential part of the sleep cycle.

It involves three stages: N1, N2, and N3, with N3 being the deepest.

NREM sleep stages are vital for physical and mental restoration.

Sleep deprivation and fragmented sleep can limit your amount of time spent in NREM sleep and lead to health problems.

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

The pons is a crucial region for the generation of REM sleep. It contains a complex variety of cells, including cholinergic, monoaminergic, GABAergic and glutamatergic neurons. The pons is necessary and sufficient for the generation of REM sleep. The pons contains a core circuitry generating 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 hypothalamus, midbrain, and medulla regulate REM sleep by either promoting or suppressing this brain state

The hypothalamus, a peanut-sized structure deep inside the brain, contains groups of nerve cells that act as control centers affecting sleep and wakefulness. Within the hypothalamus is the suprachiasmatic nucleus (SCN), which receives information about light exposure directly from the eyes and controls our behavioural rhythm.

The midbrain, which is part of the brainstem, controls the transitions between wake and sleep. Sleep-promoting cells within the midbrain produce a brain chemical called GABA, which reduces activity in the hypothalamus and the brainstem. The brainstem also plays a special role in REM sleep, sending signals to relax muscles to prevent us from acting out our dreams.

The medulla, another part of the brainstem, contains populations of neurons that regulate REM sleep by either promoting or suppressing this brain state. The medulla contains inhibitory REM-on populations, which promote REM sleep by inhibiting REM-off neurons in the ventrolateral periaqueductal gray (vlPAG).

The discovery of these populations was facilitated by the availability of novel technologies for the dissection of neural circuits

The regulation of neural messages during REM sleep is a complex process that involves various neural circuits and neurotransmitters. While the exact mechanisms are not fully understood, several studies have provided insights into the role of specific neurons and brain regions in modulating REM sleep.

The discovery of these neural populations and their functions has been greatly facilitated by advancements in technologies for the dissection of neural circuits. One such technology is optogenetics, which involves the use of light to control the activity of specific neurons. For example, optogenetic inhibition of MCH neurons and knockout of MCH receptors have been shown to block the increase in REM sleep typically observed during warm ambient temperatures (Komagata et al., 2019). This suggests that the MCH system adjusts the amount of REM sleep based on external environmental factors.

Another powerful technology for neural circuit dissection is chemogenetics, which allows for the activation or inhibition of specific neurons using designer receptors exclusively activated by designer drugs (DREADDs). Chemogenetic activation of GABAergic neurons, for instance, has been found to block the rebound of REM sleep during recovery sleep after a period of REM sleep deprivation (Hayashi et al., 2015). This indicates that activating these neurons may eliminate the homeostatic need for REM sleep.

In addition to optogenetics and chemogenetics, advancements in molecular biology, cell biology, synthetic biology, and virus studies have led to the development of various genetic tools for neural circuit dissection. These include transneuronal tracers, such as chemicals, proteins, and neurotropic viruses, which have been extensively used to study neural circuits (Schwab et al., 1979; Fujisawa and Jacobson, 1980; Itaya and van Hoesen, 1982; Kelly and Strick, 2000; Enquist, 2002). Moreover, the development of gene-editing methods like CRISPR/Cas has enabled the precise generation of gene-modified monkey models for neuroscience research.

Overall, the availability of these novel technologies has revolutionized the field of neuroscience, providing valuable insights into the neural populations and circuits involved in regulating REM sleep. By utilizing these tools, researchers can continue to unravel the complex mechanisms underlying the blocking of neural messages during REM sleep and its implications for brain function and behaviour.

Recent quantitative models integrate findings about the activity and connectivity of key neurons and knowledge about homeostatic mechanisms to explain the dynamics underlying the recurrence of REM sleep

Recent quantitative models have been developed to explain the neural and homeostatic processes governing the regulation of REM sleep. These models integrate findings about the activity and connectivity of key neurons with knowledge of homeostatic mechanisms to explain the dynamics underlying the recurrence of REM sleep.

One of the first quantitative models describing the dynamics underlying the sleep cycle was the Reciprocal Interaction Model proposed by McCarley and Hobson in 1975. This model reproduced the activity of two populations of neurons with opposing firing patterns relative to REM sleep, which had been recorded in the pontine gigantocellular tegmental field.

Subsequent research has built upon this foundation, with studies focusing on the role of specific neurons and brain regions in regulating REM sleep. For example, Kantor et al. (2009) found that lesioning orexin/hypocretin neurons led to an increase in REM sleep during the dark period, suggesting that these neurons suppress REM sleep during the active phase. Additionally, optogenetic inhibition of MCH neurons and knockout of MCH receptors have been shown to block an increase in REM sleep typically observed during warmer ambient temperatures (Komagata et al., 2019). This indicates that the MCH system adjusts the amount of REM sleep in response to external environmental needs.

Furthermore, chemogenetic activation of GABAergic neurons after REM sleep deprivation has been found to block the rebound of REM sleep during recovery sleep, suggesting that activating these neurons may eliminate the homeostatic need for REM sleep (Hayashi et al., 2015). Additionally, in cats, REM sleep deprivation reduced the activity of presumed noradrenergic REM-off neurons in the LC, potentially facilitating transitions into REM sleep under conditions of increased REM sleep pressure (Mallick et al., 1990).

By combining quantitative and experimental approaches to test model predictions and refine existing models, researchers aim to advance our understanding of the complex neural and homeostatic processes that govern the regulation of REM sleep.

Combining quantitative with experimental approaches to directly test model predictions and to refine existing models will advance our understanding of the neural and homeostatic processes governing the regulation of REM sleep

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.

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