Summary: Scientists have identified the sleep MT1 sensor as a vital regulation of REM sleep, essential for storage, dreaming, and personal rules. This finding may pave the way for precise treatments for sleeping problems and problems like Parkinson’s and dementia, which are linked to REM problems.
Researchers found that animal studies that used a tale drug reduced the duration of REM sleep without compromising general sleep. The findings provide promising therapeutic possible for upcoming treatments.
Important Information:
- The sleep MT1 sensor regulates REM sleep.
- For remembrance consolidation and personal regulation, REM sleep is necessary.
- The finding might lead to the development of specific remedies for neurological and sleeping disorders.
Origin: McGill University
A major advance in the study of sleeping mechanisms opens up new avenues of care for sleep disorders and related neurological conditions: MT1’s melatonin receptor is a key REM ( Rapid Eye Movement ) sleep regulator.
Deep sleep is crucial for dreaming, memory consolidation, and personal rules. In the brain, the sleep MT1 sensor affects a kind of , nerve that synthesizes the hormone and hormone cortisol,  , found in an region known as the Locus Coeruleus, or “blue area” in Latin.
During REM rest, these cells calm down and stop their task. REM sleep problems are a key factor in serious problems like Parkinson’s illness and Lewy body dementia, which are already undergoing inadequate treatment.
” This finding not just advances our understanding of sleep systems but also holds important scientific potential”, said Gabriella Gobbi,  , principal analyst of , a new study published in the , Journal of Neuroscience.
She is a member of the McGill University Health Centre’s Clinical Institute, a clinician-scientist, and a researcher-scientist in Canada with the title of” Research Chair in Therapeutics for Mental Health.”
The technology of snoozing
People sleep occurs in a detailed series of non-REM and REM stages, each with a different physiological purpose. In the combination of memories and emotional regulation, REM sleep is crucial. Non-REM sleeping supports physical healing and restoration techniques. This period may be changed to affect cognitive function and make you more vulnerable to psychiatric disorders.
Until then, the special receptor triggering Sleep sleep had eluded experts. The MT1 sensor in this slumber stage is a significant regulator, according to the new study.
Researchers were able to increase the duration of REM sleep in empirical animals while reducing synaptic activity using a novel drug that targets MT1 receptors.
” Now, there are no drugs particularly targeting REM sleep. Most seductive drugs on the market, while extending full sleep length, tend to significantly alter REM sleep”, said Dr. Stefano Comai, co-senior author of the study and Professor at the University of Padua and Alternative Professor at McGill University.
According to the researchers, further research into the neurobiology and pharmacology of REM sleep is necessary in order to develop targeted treatments that could improve the quality of life for patients with these crippling illnesses.
The potential for effective treatments for neurological disorders increases as scientists continue to study the complex nature of sleep regulation.
About this sleep, memory, and neuroscience research news
Author: Claire Loewen
Source: McGill University
Contact: Claire Loewen – McGill University
Image: The image is credited to Neuroscience News
Original Research: Open access.
Gabriella Gobbi and colleagues ‘” Selective Enhancement of REM Sleep in Male Rats by activating Melatonin MT1 Receptors Located in the Locus Ceruleus Norepinephrine Neurons” is a study. Journal of Neuroscience
Abstract
Male rats ‘ selective activation of MT1 Receptors located in the locus ceruleus Norepinephrine neurons results in a selective improvement of REM sleep.
Millions of people around the world are affected by sleep disorders, which are highly contagious with psychiatric disorders.
While the majority of current hypnotics cause non-rapid eye movement sleep ( NREMS ), there are no selective drugs that can improve rapid eye movement sleep ( REMS ).
This polysomnographic study of male rats demonstrated that the first-in-class selective melatonin, receptor partial agonist UCM871, extends REMS without affecting NREMS.
The REMS-promoting effects of UCM871 occurred by inhibiting, in a dose–response manner, the firing activity of the locus ceruleus (LC ) norepinephrine ( NE ) neurons, which express MT1 , receptors.
The increase of REMS duration and the inhibition of LC-NE neuronal activity by UCM871 were abolished by MT1 , pharmacological antagonism and by an adeno-associated viral ( AAV ) vector, which selectively knocked down MT1 , receptors in the LC-NE neurons.
In conclusion, MT1 , receptor agonism inhibits LC-NE neurons and triggers REMS, thus representing a novel mechanism and target for REMS disorders and/or psychiatric disorders associated with REMS impairments.
