How Sleep Loss Activates Scavenger Cells Within the Brain

Astrocytes and Microglial Cells Clear Away Neuron Connections

Sleep loss may affect brain function by activating astrocytes and microglial cells to clear away neuron connections
Michel Tcherevkoff/Getty Images

Research continues to unravel some of the mysteries of sleep. Clinical understanding may occur decades—or even centuries—before science can explain the phenomena. As an example, we know that sleep deprivation has negative impacts on the function of the brain and body. Scientific research is helping us to better understand why.

One study suggests that sleep loss may promote the activation of cells within the brain, including astrocytes and microglial cells, that scavenge and clear away the connections between neurons.

Explore the science behind this discovery, what it means to human brains, and what might be done to protect the function of the brain by ensuring adequate rest.

The Impacts of Sleep Deprivation

Since the late 1800s, studies have shown that sleep deprivation can cause significant harm to an organism. Research in dogs showed that chronic sleep deprivation led to death in a matter of days. Though the outcome was clear, the mechanism was not.

Over the past decades, the field of sleep research has blossomed, but there are many mysteries that remain to be solved. It seems that new studies make a splash on a nearly weekly basis. It is important to understand these papers in the context of the broader scientific literature. This may not always be easy, especially when the language used seems at times indecipherable. Take a moment to review some of these research findings and consider what meaning can be derived.

Studying Sleep Loss in Mice Brains

Let’s explore a study on the role of sleep loss and the impacts on the cells within the brains of mice. The anatomy and physiology of mice do not correlate perfectly with humans, but the advantages as research subjects are obvious. Advances in medical research often rely on these mouse models.

In a paper in the Journal of Neuroscience titled “Sleep Loss Promotes Astrocytic Phagocytosis and Microglial Activation in Mouse Cerebral Cortex,” Michele Bellisi and colleagues discuss changes that occur within the brain in both acute and chronic sleep deprivation. These researchers have been examining the cells of the brain and how sleep impacts their function for years.

There are a few basic terms that need to be understood to appreciate their findings. The brain has a number of important cells. Neurons are the key players, functioning through electrochemical connections in myriad ways. There is also a group of support cells within the brain called glial cells. These include astrocytes, star-shaped cells that envelop other cells and create membranes and also play a role in metabolism. Microglia are also glial cells and function as scavenger cells. They are phagocytes (literally, “eat cells”) that clean up debris within the brain. Activation of these cells within the brain can cause inflammation.

The researchers have previously learned that there are certain genes (called Mertk and its ligand Gas6) within astrocytes that are activated after acute sleep deprivation. When wakefulness is prolonged, these cells seem to engage in phagocytic activity.

Research has demonstrated that sleep deprivation leads to inflammation within the body, but it was unknown if these changes also occur within the brain.

Bellisi’s research group examined the impacts of sleep deprivation on mice brains by using a scanning electron microscope and tissue samples taken from the frontal cortex. They looked at several states: spontaneous wakefulness, after six to eight hours of sleep, acute sleep deprivation, and chronic (approximately five days) of sleep deprivation. The researchers measured the volumes within the synapses—the gaps between neurons—and the nearby processes extending from neighboring astrocytes.

How Do Brain Cells Change With Sleep Deprivation?

It was discovered that astrocytes increased their phagocytosis in both acute and chronic sleep loss. These cells consumed the components of large synapses, especially on the presynaptic side of the connections. An increase in MERTK expression and the metabolism of lipids (called peroxidation) supported this activity. What does this mean to the brain’s integrity?

The phagocytosis of astrocytes in sleep deprivation may represent how the brain’s tissues respond to the increase of synaptic activity that is associated with prolonged wakefulness. Recall that sleep deprivation is not just the absence of sleep; it is the sustenance of wakefulness. This is a process that requires energy, and one that produces waste products. The astrocytes must clear worn components of heavily used synapses.

Chronic sleep deprivation in the mice resulted in microglial activation. These cells were basically called into service to phagocytize elements of the synapse, like a custodian crew summoned to clean up a big mess. Though there were not obvious signs of inflammation within the cerebrospinal fluid surrounding the brain, the presence of these cells in the brain tissue is concerning. It is possible that an additional insult to the brain could more likely lead to an exaggerated, abnormal response by these cells, possibly contributing to brain damage. As a result, chronic sleep loss may predispose the brain to permanent problems.

The Impacts of Sleep Deprivation on Long-term Health

It is perhaps most concerning that these researchers demonstrated that just a few hours of sleep deprivation led to an increase in activity among the astrocyte cells. When the sleep deprivation was extended, the activity increased further and microglial cells were also activated. These housekeeping functions may help to support strong synapses within the brain.

Unfortunately, chronic sleep deprivation may be like other stressors, and leave the brain susceptible to damage and degeneration, perhaps even leading to states like dementia.

How to Avoid the Effects of Sleep Deprivation

It is concerning to imagine that sleep deprivation may be causing permanent damage to your brain. What can be done?

In order to avoid the effects of sleep deprivation, ensure that you are meeting your sleep needs. On average, an adult needs seven to nine hours of sleep in order to feel rested. Older adults may need a little less sleep. If you fall asleep quickly, spend little time awake at night, and feel sleepy during the day (especially with naps), you may not be getting adequate sleep.

Beyond quantity, ensure that you are getting optimal sleep quality. The sleep should be restful. If you have any symptoms of sleep disorders, like sleep apnea or insomnia, get the help that you need to resolve these conditions. Do not rely on sleeping pills beyond a few weeks as these are not a substitute for normal sleep.

By improving your sleep, this will help to ensure that you get the benefits of a good night’s rest without needing to worry about the long-term consequences of inadequate sleep.

A Word From Verywell

Scientific research supports our understanding of how the body works, but it is not infallible. It is important to remember that findings may conflict with prior knowledge, and new studies may cast a matter in a new light.

Science is a conversation, an ongoing pursuit of the truth. If this study encourages you to optimize your sleep, it has value to your health, but it should not raise undue concern about sleep loss that has occurred in the past. That ship has sailed. Focus on what you can do today and to benefit your long-term well-being moving forward.

Sources:

Bellisi M, et al. “Sleep Loss Promotes Astrocytic Phagocytosis and Microglial Activation in Mouse Cerebral Cortex.” Journal of Neuroscience. 24 May 2017; 37(21):5263-5273.

Bentivoglio M and Grassi-Zucconi G. "The pioneering experimental studies on sleep deprivation." Sleep. 1997 Jul;20(7):570-6.

Fix, JD. High-Yield Neuroanatomy. 2nd edition. Philadelphia: Lippincott, Williams, & Wilkins, 2000, pp. 30-32.

Purves D, et al. Neuroscience. 3rd edition. Sunderland, Mass.: Sinauer Associates, Inc., 2004, pp. 8-9.

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