Summary: Researchers who study the little round worm C. Elegans have discovered a surprising mechanism by which a single cerebral signal controls both falling asleep and waking up. The Chemical Messenger FLP-11 activates a receiver called DMSR-1 in different neurons to silence the awakening or stop sleep, acting as an on-off biological switch.
This double function helps to regulate not only the initiation of sleep, but also its duration. The discovery could shed light on future research on sleep disorders such as insomnia and narcolepsy in humans.
Key facts:
- Unique molecule, double role: FLP-11 induces and ends sleep C. Elegans By acting on different neurons.
- Discovery of receivers: The DMSR-1 receiver is essential to interpret the sleep commands of the FLP-11.
- Wider relevance: Although studied in verses, this mechanism can reveal sleeping ways preserved through species, including humans.
Source: Tud
People spend about a third of their sleeping life. However, we know surprisingly about how our brains control is falling asleep and waking up.
Now, researchers led by Professor Henrik Bringmann at the Biotechnology Center (Biotec) of the University of Technology of Tud Dresden discovered another piece of this puzzle. The team has shown that a single cerebral signal acts as a biological switch – both triggering sleep and finishing.
Their results, published in the journal Current biologywere made possible by studying a small round worm C. Elegans, a powerful model organism in biology.
“It is really important to be able to fall asleep, but just as important to wake up too!”, Explains Professor Bringmann, research group manager at Biotec who led the study.
“We know that falling asleep and wake up is controlled by a special set of brain cells, called sleep neurons. However, we do not know exactly how they control the molecular tracks downstream to make us fall asleep and wake us up again.
The Bringmann group turned to C. ElegansA little round worm to answer these questions. Unlike humans, who have thousands of sleep neurons that control sleep, C. Elegans needs a single neuron to do this job. This simplicity makes it a perfect model organism to study the main molecular pathways controlling sleep.
This research highlights one of the fundamental questions in biology: how organisms regulate sleep and awakening. By understanding fundamental molecular machines behind sleep, researchers can better understand sleep disorders such as narcolepsy and insomnia which have a major impact on quality of life.
The results also add to the growing number of evidence that even simple model organisms can reveal fundamental mechanisms that govern life.
A molecule, two jobs
The team focused on a chemical messenger called FLP-11. When a sleep neuron activates, it releases the FLP-11. These chemical messengers work as molecular “notes” that have placed between brain cells to deliver different commands.
“We knew that the FLP-11 is essential for sleeping, but we did not know what message it transmits and to whom,” explains Professor Bringmann.
Thanks to genetic screening, the researchers identified a key receiver, called DMSR-11, that FLP-11 binds to transmit its message. If this receiver was missing in the brain, the researchers observed that worms were sleeping much less. DMSR-1 has proven to be present in different types of neurons.
According to the neuron received the message, the results were considerably different.
“We have discovered that the FLP-11 activates the DMSR-1 receptors in two completely different types of neurons,” explains Lorenzo Rossi, a doctoral student who led the experiences in Professor Bringmann’s laboratory.
“We found the receiver present in neurons that promote awakening. When activated by the FLP-11, the receiver deactivates the neurons of the awakening.
“This, in turn, helps the worm to fall asleep. On the other hand, the receiver is also present in the sleep neuron itself. Here, he also extinguishes it, which finally awakens the animal, ”explains Lorenzo Rossi.
In other words, the same chemical product that puts the green asleep also helps to wake it again, simply by targeting different cells in the brain.
“This is an effective mechanism that controls the start of sleep while keeping its duration in check,” adds Professor Bringmann.
A universal principle?
“Unlike humans, C. Elegans have much shorter sleep phases that last only about 20 minutes. However, sleep is a fundamental biological process that many molecules and mechanisms involved in sleep are shared between species, ”explains Professor Bringmann.
“We do not yet know if the same sleep switch exists in humans, but it provides a promising index in the search for mechanisms that control sleep in our species.”
About this news of sleep and neuroscience research
Author: Magdalena Gonciarz
Source: Tud
Contact: Magdalena Gonciarz – Tud
Picture: The image is credited with Neuroscience News
Original search: Open access.
“”The neuropeptide FLP-11 induces and inhibits auto-inhibits through the DMSR-1 receiver Caenorhabditis ElegansBy Henrik Bringmann et al. Current biology
Abstract
The neuropeptide FLP-11 induces and inhibits auto-inhibits through the DMSR-1 receiver Caenorhabditis Elegans
Sleep is caused by the depolarization of active sleep neurons, which secrete gamma-aminobutyric acid (GABA) and neuropeptides such as the preserved RFAMIME (C-Terminal Arg-Phe-NH2 Pattern) Neuropeptides to dictate when an organism falls asleep and when it wakes up.
However, the mechanisms by which the neurotransmission of active sleep neurons induces sleep and determines that the duration of sleep remains poorly understood. Get into Caenorhabditis Elegans Crucially requires the unique and active sleep neuron of sleep, which induces sleep via the release of Neuropeptides Rfamide FLP-11.
However, the way RIS and FLP-11 control sleep is not well understood, as the receiver by which FLP-11 acts has not yet been identified. In this study, we discovered that RIS and FLP-11 control sleep through the GE / S-Protein receiver coupled receiver of the receiver of the Dromyosuppressine 1 receiver (DMSR-1).
Using Knockdowns specific to cells, we will demonstrate that DMSR-1 induces sleep by acting in cholinergic neurons downstream of the activation of RIS. Pharmacological intervention indicates that the inhibition of cholinergic signaling is necessary for sleep.
Consistently, the expression of DMSR-1 in cholinergic neurons is essential for central sleep functions, including the expression and survival of protective genes. On the other hand, we found that DMSR-1 In the RIS, the control of negative feedback during sleep limits the activation of the Ris calcium and the duration of the sleep. Therefore, DMSR-1 In Ris inhibits the expression and survival of protective genes.
Thus, DMSR-1 controls both the initiation and the limitation of sleep, effectively coupling sleep induction with a sleep signal.
The signaling of neuropeptide-GPCR RFAMIDE could underlie double similar sleep control mechanisms in other species, and the self-inhibition of active sleep neurons could represent a mechanism kept to limit the duration of sleep.
