What's the point of sleep?

What's the point of sleep?

Almost as much as eating food or tormenting the local wildlife, my cats love to sleep. Which is probably why I get on so well with them, because I'm also quite partial to a good nap. The trouble with sleep is that no one's quite sure why we actually do it. But a new paper published in the Journal of Neuroscience provides clues pointing towards one possible function – sleep might help to repair support structures in the brain.

Chiara Cirelli and colleagues at the University of Wisconsin-Madison looked at the sleeping patterns of transgenic mice, which were modified to express a green fluorescent protein in a specific type of brain cell called an oligodendrocyte. Oligodendrocytes act as a sort of insulating scaffold structure for neurons. Located in the brain and spinal cord, they attach to the axon – the long fibre that extends out of the neuron's cell body and ends in a terminal that connects to other neurons – and produce a coating of fat and protein called the myelin sheath.

For neurons to function properly, myelin is extremely important. The presence of myelin allows impulses to "hop" along the axon, increasing the overall speed at which information is transmitted to other cells. If a neuronal axon wasn't covered in myelin, electrical impulses generated by the cell body would basically leak out into the surrounding fluid, resulting in a slower transfer of information from one neuron to another. Progressive loss of myelin is a key factor in multiple sclerosis, and can result in vision loss, limb weakness, memory loss and fatigue, among other things.

Cirelli's team were interested in gene expression in oligodendrocytes. When a gene is expressed, it plays a part in activating or deactivating what a particular cell can do – think of it like a switch that kickstarts different cellular functions. While we generally know that lots of genes are activated during different periods of the sleep wake cycle, we know less about how sleep affects specific cell types. So by figuring out which genes in oligodendrocytes are activated at different times in the sleep and wake cycle, Cirelli's team was able to understand more about the role that sleep plays in changing and regulating the activity in these key support structures.

They found that in mice that had been asleep, genes involved in creating myelin, or promoting the production of oligodendrocyte precursor cells, showed greater activation. On the other hand, for mice that were awake or had been sleep-deprived, there was greater activation of genes involved in cellular stress responses and cell death. In other words, sleep appears to promote the reproduction of cells that are essential in helping the brain to repair itself.

How does this fit in with other theories of sleep? One, called the repair and restoration theory, argues that sleep (especially REM sleep) helps to restore physiological resources that have been depleted throughout the day. In line with this, Cirelli's team found that the more time the mice spent in REM sleep, the more the oligodendrocyte precursor cells proliferated.

But while this all fits together, there are a lot of findings that contradict the repair and restoration theory. For example, on the basis of this theory, you might presume that the more active you are, the more sleep you need. But this doesn't seem to be the case. Furthermore, in assuming that there is only a single purpose for sleep, it ignores the fact that sleep patterns vary wildly across different species, and even between members of the same species.

An alternative suggestion that tries to take into account these differences is known as the evolutionary, or energy conservation, theory. The idea here is that animal species vary in their sleep habits in ways that make sense if you look at how many hours they need to be awake. For example, grazing animals, which need to eat for a large portion of the day, get less sleep than carnivores that can satisfy their nutritional needs with a single meal. Similarly, animals that need to be alert for predators get little sleep, and vice versa. It's difficult to see how the results from Cirelli's study fit with a theory like this, as it doesn't really explain why we have REM and non-REM sleep, for instance.

One thing that is worth pointing out is that Cirelli's study, on transgenic mice, is still a far cry from understanding the possible functions of human sleep. So while it's tempting to suggest from this study that chronic poor sleep might be a contributing factor to diseases such as multiple sclerosis, we're still quite a way off making that link between human sleep patterns, support cell reproduction, and neurodegenerative disorders. In the meantime, though, just to be on the safe side, I'm off for a nap.

By Pete Etchells

The Guardian, 5 September 2013

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