During REM sleep, our eyes move back and forth, but our bodies remain still. This phenomenon, known as REM atonia, is a form of temporary muscle paralysis that prevents us from acting out our dreams. While the exact mechanism behind REM sleep paralysis is not fully understood, recent research has provided valuable insights. Studies on mice have identified a group of neurons in the brainstem, specifically in the ventral medial medulla, that suppresses unwanted movements during REM sleep. These neurons are connected to those controlling voluntary movements but not eye or internal organ muscles. When the input to these neurons is blocked, mice start moving during sleep, resembling the behaviour seen in people with REM sleep behaviour disorder. This discovery offers promising avenues for developing treatments for sleep disorders such as narcolepsy, cataplexy, and REM sleep behaviour disorder.
Characteristics | Values |
---|---|
Part of the brainstem that paralyzes us during REM sleep | Neurons in the brainstem |
Location of these neurons | Ventral medial medulla |
Input from | Sublaterodorsal tegmental nucleus (SLD) |
Type of neurons | Inhibitory |
Function | Prevent muscle movement when active |
What You'll Learn
- Neurons in the brainstem suppress movement during REM sleep
- REM sleep behaviour disorder is caused by a breakdown in communication between neurons
- The subcoeruleus nucleus is the core of the REM-generating circuit
- The glycinergic neurons in the ventromedial medulla could be targeted for drug therapies
- REM sleep behaviour disorder could be an early marker of neurodegenerative diseases
Neurons in the brainstem suppress movement during REM sleep
During REM sleep, the brainstem suppresses movement, ensuring our bodies remain still as our eyes move back and forth. This state of near-paralysis is known as REM atonia and is a well-documented phenomenon in sleep science.
A group of researchers at the University of Tsukuba in Japan discovered a set of neurons in the mouse brainstem that are responsible for suppressing movement during REM sleep. These neurons, located in the ventral medial medulla, are connected to neurons that control voluntary movements. When the input to these neurons was blocked, the mice began to move during sleep, resembling the movements of someone with REM sleep behaviour disorder.
The researchers, led by Professor Takeshi Sakurai, also found that these neurons were inhibitory, meaning they can prevent muscle movement when active. This discovery could be significant for developing treatments for sleep disorders such as narcolepsy, cataplexy, and REM sleep behaviour disorder.
REM sleep behaviour disorder is characterised by a loss of normal muscle paralysis during REM sleep, resulting in movement and even injury to oneself or others. The suppression of movement during REM sleep is, therefore, a crucial function of the brainstem, preventing us from acting out our dreams.
The brainstem, composed of the pons, medulla, and midbrain, plays a critical role in controlling the transitions between wakefulness and sleep. It is also involved in sending signals to relax muscles essential for body posture and limb movements during REM sleep.
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REM sleep behaviour disorder is caused by a breakdown in communication between neurons
The brainstem plays a crucial role in regulating sleep, controlling the transitions between wakefulness and sleep. During REM sleep, the brainstem sends signals to relax muscles essential for body posture and limb movements, preventing us from acting out our dreams.
REM sleep behaviour disorder (RBD) is a chronic sleep condition characterised by dream enactment and a loss of REM atonia. Individuals with RBD act out their dreams, often engaging in violent movements that can result in injury to themselves or their bed partners. This disorder is caused by a breakdown in communication between neurons, specifically those involved in suppressing unwanted movements during REM sleep.
Recent studies have identified a group of neurons in the mouse brainstem that are responsible for suppressing movement during REM sleep. These neurons are located in the ventral medial medulla and receive input from the sublaterodorsal tegmental nucleus (SLD). When input to these neurons is blocked, mice exhibit movement during sleep, similar to the behaviour observed in individuals with RBD.
The primary cause of RBD is believed to be an excitation/inhibition imbalance in the brainstem nuclei that control REM muscle tone. This imbalance leads to a disinhibition of neurons, resulting in muscle activity during REM sleep. Additionally, abnormal disinhibition in the pyramidal motor tract during REM sleep may contribute to the execution of complex movements.
The breakdown in communication between neurons in RBD can have several underlying causes. In some cases, it may be associated with the use of certain antidepressant medications, such as SSRIs, which can interfere with REM atonia. RBD can also occur secondary to other sleep disorders like narcolepsy or neurological lesions affecting sleep/wake regulatory brain regions.
The treatment of RBD focuses on creating a safe sleep environment and managing symptoms. Pharmacological interventions, such as clonazepam and melatonin, are often used to enhance inhibitory processes within the brain and reduce motor behaviours during sleep. However, the long-term use of benzodiazepines like clonazepam should be carefully considered due to potential side effects and the risk of cognitive impairment.
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The subcoeruleus nucleus is the core of the REM-generating circuit
The subcoeruleus nucleus (SubC) is a core region of the brainstem that is active during REM sleep. It is also known as the sublaterodorsal nucleus. The SubC is composed of REM-active neurons, which are predominantly active during episodes of REM sleep. The majority of these neurons are glutamatergic, suggesting that REM sleep is generated by a glutamatergic mechanism. However, GABA SubC cells have also been implicated in REM sleep control.
The SubC is involved in the generation of REM sleep and is located at the mesopontine junction, medial to the trigeminal motor nucleus and ventral to the locus coeruleus. The SubC receives glutamatergic input, which may be involved in the activation of SubC neurons during REM sleep.
REM sleep is characterised by rapid eye movements, cortical activation, vivid dreaming, skeletal muscle paralysis (atonia), and muscle twitches. The SubC is thought to induce REM sleep muscle paralysis by recruiting GABA/glycine neurons in the ventromedial medulla (VMM) and spinal cord. These cells produce motor atonia during REM sleep by inhibiting skeletal motoneurons.
The SubC is also implicated in the sleep disorder cataplexy, which is the sudden and involuntary reduction or loss of skeletal muscle tone during wakefulness. Cataplexy is thought to result from the intrusion of REM sleep paralysis into wakefulness.
The SubC is a crucial component of the REM-generating circuit, and its dysfunction can lead to common REM sleep disorders such as cataplexy and REM sleep behaviour disorder (RBD).
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The glycinergic neurons in the ventromedial medulla could be targeted for drug therapies
During REM sleep, the brainstem, specifically the pons, medulla, and midbrain, plays a crucial role in suppressing unwanted movements and relaxing muscles essential for body posture and limb movements. This prevents us from acting out our dreams. Within the brainstem, the ventromedial medulla (VMM) is particularly important for inducing muscle atonia during REM sleep. The VMM contains glycinergic neurons that are connected to neurons controlling voluntary movements but not those governing eye or internal organ muscles. These glycinergic neurons are inhibitory, meaning they can prevent muscle movement during REM sleep.
The discovery of these glycinergic neurons in the VMM has significant implications for drug therapies targeting sleep disorders such as narcolepsy, cataplexy, and REM sleep behaviour disorder. By understanding the role of these neurons in suppressing muscle movement during REM sleep, researchers can explore therapeutic interventions to modulate their activity. This could involve developing drugs that act on the VMM to regulate the activity of these glycinergic neurons, potentially reducing the symptoms associated with these sleep disorders.
The VMM has also been implicated in the development and maintenance of chronic pain. Neurons in the VMM, particularly the rostral ventromedial medulla (RVM), are part of the brainstem regulatory pathway that contributes to chronic pain. While targeted drugs are a promising approach for chronic pain management, the development of new drugs targeting the RVM and related pathways has been challenging due to the complex roles of the RVM in pain regulation. However, ongoing research aims to elucidate the exact mechanisms by which the RVM contributes to chronic pain, which could inform the development of novel drug therapies.
Furthermore, the VMM plays a crucial role in regulating arterial pressure. The RVM, in particular, contains μ-opioid-expressing neurons that are involved in maintaining neuropathic pain. Ablation or inhibition of these neurons has been shown to reduce the duration of allodynia and hyperalgesia caused by nerve injury. This suggests that targeted interventions, such as drug therapies, aimed at modulating the activity of these neurons could be explored to manage chronic neuropathic pain effectively.
In summary, the glycinergic neurons in the ventromedial medulla could be promising targets for drug therapies aimed at treating sleep disorders and chronic pain conditions. By understanding the role of these neurons in suppressing muscle movement during REM sleep and their involvement in pain regulation, researchers can develop targeted interventions to modulate their activity and improve patient outcomes. Further studies are needed to fully elucidate the complex functions of the VMM and its glycinergic neurons, which will ultimately inform the development of effective drug therapies.
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REM sleep behaviour disorder could be an early marker of neurodegenerative diseases
REM sleep behaviour disorder (RBD) is a sleep disorder characterised by dream enactment and loss of REM atonia. During the REM stage of sleep, the body is usually temporarily paralysed, but people with RBD may act out their dreams physically and vocally, sometimes violently, and can cause injury to themselves or their bed partner. RBD is considered a parasomnia, a sleep disorder that involves unusual and undesirable physical events or experiences that disrupt sleep.
RBD is strongly associated with certain neurodegenerative disorders. About 97% of people with isolated or idiopathic RBD will go on to develop a neurodegenerative condition within 14 years of diagnosis, such as Parkinson's disease, Lewy body dementia or multiple system atrophy (MSA). These conditions are called alpha-synucleinopathies. As such, RBD is considered a prodromal stage of an alpha-synucleinopathy, and can be an early warning sign of these conditions.
The brainstem plays a role in controlling transitions between wake and sleep. During REM sleep, the brainstem sends signals to relax muscles essential for body posture and limb movements, so that we don't act out our dreams. A specific group of neurons in the brainstem called the ventral medial medulla (VMM) plays an important role in inducing muscle atonia during REM sleep. The VMM receives input from another area of the brainstem called the sublaterodorsal tegmental nucleus (SLD). When the input to these neurons is blocked, the body is no longer paralysed during sleep.
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Frequently asked questions
REM stands for rapid-eye movement sleep. It is the deep sleep stage where most recalled dreams occur. Our eyes continue to move but the rest of the body's muscles are paralysed, possibly to prevent injury.
REM atonia is the technical term for the paralysis of muscles during REM sleep.
REM sleep paralysis is caused by neurons in the brainstem that suppress unwanted movement. These neurons are located in an area of the brain called the ventral medial medulla and receive input from another area called the sublaterodorsal tegmental nucleus, or SLD.
REM sleep behaviour disorder is a sleep disorder where people act out their dreams, often violently. This can cause serious injuries to the patient and those around them. It is also often an early indicator of neurodegenerative diseases, such as Parkinson's.