Summary: Researchers have discovered two neuron forms in the brain that trigger REM sleep, shedding light on the mechanisms underlying this critical sleep stage. These cells form circuits that power mind activity, eye movements, and body strengthen loss during REM sleep.
Similar to those in individuals with Parkinson’s disease, REM sleep behavior abnormalities were caused by the inhibition of these neurons in mice, suggesting a strong connection between nerve damage and the problem. This discovery may lead to novel therapies for degenerative diseases like Parkinson’s and sleep disorders.
Important Information:
- Two different brainstem neurons control the important characteristics of the brainstem and cause REM sleep.
- Inhibiting these cells caused Deep slumber defects related to Parkinson’s symptoms.
- Findings may help to develop more effective treatments for neurological disorders and REM sleep disorders.
Origin: University of Tsukuba
During REM sleep, goals are often seen. The training of REM nap was not well understood. Several diseases are preceded by abnormalities in REM sleep.
Importantly, REM sleep behavior disorder, in which individuals literally act out goals by moving and vocalizing during REM sleep, has been noted as an early sign of degenerative diseases, such as Parkinson’s disease.
These anomalies were unrelated to their causes.
Herein, researchers identified two neuron types in the brainstem ( pons and medulla oblongata ) that induce REM sleep. These neurons create circuits that connect to brain regions that control the rapid eye movements, cerebral cortex activation, and muscle tone loss, all hallmarks of REM sleep. Even in awake mice, the artificial activation of this circuit causes a strong REM sleep.
In addition, the induction of these REM sleep-inducing cells in mice resulted in abnormalities similar to those seen in Parkinson’s disease, including significant body movements while REM sleep is being REM sleep, as well as significant REM sleep reduction.
Patients with Parkinson’s disease and REM sleep behavior disorder had fewer REM sleep-inducing cells in the brainstem, revealing a cause of the disorder.
These findings should help us better understand the mechanisms and significance of REM sleep, leading to the development of novel treatment and prevention strategies for sleep disorders and related illnesses.
Funding: This work was supported by the World Premier International Research Center Initiative ( WPI), JSPS KAKENHI grant numbers JP20K22674, JP21K15179 ( to M. Kashiwagi), and JP20K06910 ( to G. B. ), MEXT KAKENHI grant numbers JP23H04210, JP23H04668 ( to Y. H. ), JP16H06280 ( to M. W. ), and JP16H06277 ( CoBiA ) ( to S. M. ), and AMED grant numbers JP22gm1110008, JP21zf0127005 ( to Y. H. ), JP22wm0425018 ( to G. B. and Y. H. ), JP21dm0207070 ( to H. M. ), JP20dm017106, and JP21wm0425019 ( to S. M. ).
About this information on neuroscience and sleep
Author: YAMASHINA Naoko
Source: University of Tsukuba
Contact: YAMASHINA Naoko – University of Tsukuba
Image: The image is credited to Neuroscience News
Original Research: Open access.
” A pontine-medullary loop crucial for REM sleep and its deficit in Parkinson’s disease” by MOCHIZUKI, Hideki et al. Cell
Abstract
A pontine-medullary loop crucial for REM sleep and its deficit in Parkinson’s disease
Due to the neuronal heterogeneity of the brainstem, it has been challenging to identify the characteristics of the rapid eye movement ( REM) sleep circuitry and its relationship to diseases.
Here, we show in mice that neurons in the pontine sublaterodorsal tegmentum ( SubLDT ) that express corticotropin-releasing hormone-binding protein ( Crhbp+ , neurons ) and project to the medulla promote REM sleep.
Within the medullary area receiving projections from , Crhbp+ , neurons, neurons expressing nitric oxide synthase 1 ( Nos1+ , neurons ) project to the SubLDT and promote REM sleep, suggesting a positively interacting loop between the pons and the medulla operating as a core REM sleep circuit.  , Nos1+ , neurons also project to areas that control wide forebrain activity.
Ablating , Crhbp+ , neurons reduces sleep and impairs REM sleep atonia. In patients with REM sleep behavior disorders, CRHBP-immunoreactive neurons are largely reduced and contain pathologic -synuclein, giving insight into the mechanisms underlying the sleep deficits that characterize this condition.
