Brain Cells We Thought Were Just Fillers Might Actually Be the Key to Our Body Clocks

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Scientists have discovered that brain cells that were once considered to be simple place-holders for neurons could actually play an important role in helping to regulate our circadian behaviour.

Astrocytes are a kind of glial cell – the support cells that are often called the glue of the nervous system, as they provide structure and protection for neurons. But a new study shows that astrocytes aren't just gap-fillers, and may be crucial for keeping time in our inner body clock.

In 2005, one of the team, neuroscientist Erik Herzog, helped figure out that astrocytes also include these clock genes.

By isolating the brain cells from rats and coupling them with a bioluminescent protein, Herzog's team showed that they glowed rhythmically – evidence that they were capable of keeping time like other cells.

It took more than a decade for the researchers to figure out how to measure the same astrocyte behaviour in a living specimen, by using CRISPR-Cas9 gene-editing to delete a clock gene called Bmal1 in the astrocytes of mice.

Left to their own devices, mice have circadian clocks that last for approximately 23.7 hours. We know this because mice in constant darkness will start running on a wheel every 23.7 hours, and usually don't miss their time slot by more than 10 minutes.

Humans also miss the 24-hour mark slightly – a Harvard University study in 1999 found that our internal clocks run a tad overlong, on a daily cycle of 24 hours, 11 minutes.

But even though Herzog had demonstrated in 2005 that astrocytes were involved in keeping time, the team didn't necessarily expect mice without Bmal1 to be affected, because most research surrounding the suprachiasmatic nuclei has demonstrated the controlling effect of neurons, not astrocytes.

But, to the researchers' surprise, deleting the clock gene in the astrocytes saw the mouse internal clocks run slower – beginning their daily run about 1 hour later than usual.
In another experiment, the team studied mice with a mutation that caused their circadian clocks to run fast. By repairing this gene in the animals' astrocytes – but not fixing the defect in their neurons – they weren't sure what the affect would be.

The findings are reported in Current Biology.