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.
