Sleepless nights make your brain overproduce connections, and not in a good way

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Krista Mangulsone, Unsplash (CC0, https://creativecommons.org/publicdomain/zero/1.0/)
Krista Mangulsone, Unsplash (CC0, https://creativecommons.org/publicdomain/zero/1.0/)

German researchers say a night without sleep can make your brain produce excess connections between its cells - known as synapses - which will then require more energy to function, leading to buildups of proteins in your head and fatigue. To figure this out, the researchers scanned the brains of 40 people, half of whom had gone one night without sleep. They say the sleep-deprived group had higher measures of synaptic vesicle glycoprotein 2A (SV2A) - a marker of brain synapses - than the group that had regular sleep. These heightened levels of SV2A were found in areas of the brain known for memory and information relay, the team say. Additionally, the researchers say that when the sleep-deprived participants were allowed a two-hour nap, they found these heightened levels of SV2A were associated with more slow-wave activity - a marker of deep sleep - suggesting our brains might be working harder to return to balance.

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From: PLOS

A sleepless night increases connections between brain cells

An increase in a marker for connections was associated with deeper sleep during later naps

A night without sleep produced increased markers of connections between brain cells, showing that sleep in humans may be important for restoring cellular balance in the brain, according to a study published June 23rd in the open access journal PLOS Biology by David Elmenhorst from the Forschungszentrum Jülich Institute of Neuroscience and Medicine in North Rhine-Westphalia, Germany, and colleagues.

Scientists have long wondered why exactly humans and other animals need to sleep. One potential mechanism is that sleep is required to restore synaptic connections and homeostasis in the brain. Synapses—the connections between brain cells—become stronger during wakefulness. This increases the amount of energy the brain needs and leads to buildup of proteins in the brain. Sleep is thought to reset these levels, reducing synaptic connections and restoring homeostasis, but evidence has thus far been limited to animal models. To determine whether the synaptic homeostasis hypothesis is supported in humans, the authors of this study used positron emission tomography (PET) to look for markers of synaptic vesicle glycoprotein 2A (SV2A), a marker of brain synapses in 40 participants, half of whom had gone one night without sleep.

The authors found that after 28 hours of continuous wakefulness, the sleep deprivation group had higher measures of SV2A in several brain regions, including the hippocampus (an area important for memory), and the thalamus, an important information relay in the brain. When the sleep-deprived participants were allowed a two-hour nap, higher levels of SV2A were associated with more slow wave activity during sleep, a marker of deep sleep and sleep pressure. While SV2A is only a proxy for brain cell connections and the elevations were relatively small, the results support the synaptic homeostasis model of sleep, and suggest a biological connection between the need for sleep and the buildup of cell connections.

The authors add, “During sleep deprivation, the brain remains awake longer and continues to process stimuli and information. Our study shows that after approximately 28.5 hours of wakefulness, a marker for synaptic density increases in several brain regions. This suggests that sleep deprivation not only causes fatigue but is also accompanied by measurable changes in neural connections.”

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PLOS Biology
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Organisation/s: Institute of Neuroscience and Medicine (INM-2), Germany
Funder: This research was supported by internal institutional funds and the project SleepLess, which received funding from the Bundesministerium für Bildung und Forschung (Federal Ministry of Education and Research, BMBF), the Fonds voor Wetenschappelijk Onderzoek - Research Foundation Flanders (FWO), and the Fonds de recherche du Québec - Santé (Quebec Health Research Fund, FRQS) under the frame of ERA-NET Neuron Cofund (grant # 01EW1808). AD received funding from public funding authorities: German Research Foundation (Grants for Collaborative Research Centre 1451 C04 and DR 445/9-1) and Wellcome Leap.
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