Did you know that when dolphins sleep they shut down only one half of their brain? The other half stays awake just in case a shark or other predator comes around.

While none of us are likely to have perfected what the dolphins can do, did you know that when we get really over tired, parts of our brain has little micro-naps while the rest of our brain is still awake?

These micro-naps are thought to be responsible for those episodes such as when someone falls asleep at the wheel while driving a car.

When we get dog-tired it is much harder to pay attention, we make more mistakes and we are far less aware of our surroundings. Have you ever had that experience when all your remaining focus is on trying to keep your eyelids open and both eyeballs focussed in the same direction? Or when you realise you have become the nodding donkey in a particularly sleep inducing presentation, and just hope that when you came too again, it’s not with a loud snort?

Some brain cells take themselves off to bed before the rest of our brain.

A new study suggests that even before we get to this stage of nodding off, certain brain cells are already in shut down mode. This means parts of our brain are already asleep while the rest is still functioning. A bit like closing down one window on your computer screen while the others remain active.

Actually, it may be that certain neurons are more affected than others when we get tired, and these are the ones that go “off-line” even when the brain on EEG is still showing a wakeful pattern.
The problem is that if certain groups of brain cells or areas are dozing wile the rest of us is still awake, this is still likely to impair our performance.

Researchers at the University of Winsconsin-Madison monitored 20 brain cells in rats to see which brain cells stayed awake when the rats were tired. Of the 20 brain cells, 18 stayed awake, but two showed signs of being asleep, with brief periods of EEG activity alternating with periods of neural silence. Plus the rats were noticed to be making mistakes. They were noticed to be less able to manouevre their paws accurately to pick up a food pellet or dropped the food pellet more frequently.

Why does our brain do this?

Why parts of our brains should take these micro-naps when we are still awake but tired has yet to be explained. Maybe it is a protective mode the brain has developed to allow those especially fatigued neurons to get the rest they need.
Maybe too it could explain why some of those more aberrant events occur when we are tired, such as when I found myself holding the dog lead and opening the fridge to put it away the other night. Or maybe there’s another reason for that!

Ref:
Vladyslav V. Vyazovskiy, Umberto Olcese, Erin C. Hanlon, Yuval Nir, Chiara Cirelli, Giulio Tononi. Local sleep in awake rats. Nature, 2011; 472 (7344): 443 DOI: 10.1038/nature10009

It has long been thought that it was only our brain cells or neurons that were actively engage in brain signalling.
It now appears that immune cells in the brain, called microglia have an important role in the creation and elimination of brain cells synapses.
Synapses are the junctions where brain cells or neurons can pass chemical signals to each other.

Microglia in their role as immune cells are known to protect the brain against infection and injury. When activated, they become able to release various inflammatory molecules, which can influence which brain cells survive. They can engulf or phagocytose and dispose of cellular debris. Now it is thought they are also involved in eliminating synapses. This new discovery suggests they have an additional role involving learning and memory.

The findings from researchers based at the University of Rochester have just been published the November 2nd edition of PLoS Biology.
Quantitative electron microscopy and two photon in-vivo imaging were used to see how microglia interact with brain synapses in the visual cortex of mice.

The researchers discovered that when there is no infection or injury for the microglia to be concerned with, they nevertheless remain very active.
Microglia are mobile and travel between the brain cell circuits.
The researchers showed how the microglia were constantly touching and wrapping around synapses, and appear to have a role in determining which stay persist and which are eliminated.

Nerve cells have what are called dendritic spines, which allow them to grow new dendrites. If was observed that if microglia touched these spines then there was a far greater chance that they would be eliminated.

The researchers also looked at the effect of modifying the external visual environment. In the absence of light, the microglia contacted more synapses and were more likely to steer towards larger dendrites, a behaviour which was reversed when the light exposure was reintroduced.

These findings are adding to our growing understanding of the role of different types of brain cells and how they interact together. The role of microglia is now being looked at in relation to disease processes such as Parkinson’s disease, Alzheimer’s, schizophrenia, obsessive compulsive disorder and possibly even autism.

Tremblay M-E, Lowery RL, Majewska AK. Microglial Interactions with Synapses Are Modulated by Visual Experience. PLoS Biology, 2010; 8 (11): e1000527 DOI: 10.1371/journal.pbio.1000527

P7C3. Remember this name!

Each week I scan different science reports from around the world, which continue to supplement our understanding of how our brain works.
Sometimes one report will leap out from the page when I read it, as it seems to herald a particularly important finding and this week I came across one such report.

The key to maintaining our ability to learn new skills and lay down memory, as we get older is dependent in part in our ability to produce new brain cells.
This is neurogenesis, one component of what makes our brain “plastic”.
The production of new baby brain cells occurs in what is called the dentate gyrus, one region of the hippocampus, which is the area of the brain, associated with learning and memory. However many of the new cells produced don’t necessarily survive to get fully incorporated into our brain.

Think of it in the same way as when turtle hatchlings are released into the ocean. Only a very small percentage actually survive and grow to adulthood. It’s the same with our brain cells. It takes several weeks for new brain cells to fully mature and most of them die off. Plus, the ability for our new brain cells to survive declines, as we get older. So researchers have been looking to identify compounds, which could enhance our newborn brain cells survival.

The results of the recent study could prove to be a breakthrough for potential treatment of Alzheimer’s disease.
A team of researchers at the University of Texas Dallas have found a compound which (at least for rodents) has been shown to increase survival rates of newly formed brain cells and by helping the rats to form new memories, reverse their memory loss.

The compound (given the really sexy name of P7C3) was one of over 1000 molecules investigated by the team. Using genetically engineered mice that lacked a gene needed to allow newborn brain cells to survive, the addition of the P7C3 reduced the expected newborn brain cell death rate.

The next step of the study then looked at whether the compound could slow down age related brain cell death and cognitive decline.
Apparently they used rats for this part of the test because it involved a water maze test, which the genetically engineered mice couldn’t do because they couldn’t swim.
(This conjures up images of mice wearing water wings. But I digress.)
The P7C3 was given on a daily basis to elderly rats with memory problems for two months and they were then subjected to the water maze task. The rats that received the P7C3 performed significantly better than the rats that had not received it. Moreover it was found that the rats given the P7C3 had three times higher than the normal level of newborn brain cells in the dentate gyrus of their hippocampus.

The conclusion was that the P7C3 enhanced new brain cell formation as well as increasing their rate of survival.

This exciting finding indicates that it may be possible in the future to be able to use compounds such as this in humans, because it can be given orally, can cross the blood brain barrier, and can produce long lasting effects for preserving memory and enhancing new brain cell survival. And the compound appears to be safe.

Obviously this is a long way off from being a substance suitable to use in humans, but it heralds an exciting development that we may have treatments in the future that could potentially address some of the core problems associated with Alzheimer’s disease where brain cell death is a marked feature.

And the team have already found that a derivative of the P7C3 called A20 appears to have an even greater neuro protective effect. A20 is apparently 300 times more potent than another compound, which is currently being used in clinical trials as a treatment for Alzheimer’s. The team are now looking to work out how these compounds, P7C3 and A20 produce their effect.
So watch this space.

Reference:
Pieper AA, Xie S, Capota E, Estill SJ, Zhong J, Long JM, Becker GL, Huntington P, Goldman SE, Shen CH, Capota M, Britt JK, Kotti T, Ure K, Brat DJ, Williams NS, MacMillan KS, Naidoo J, Melito L, Hsieh J, Brabander JD, Ready JM, McKnight SL. Discovery of a Pro-neurogenic, Neuroprotective Chemical. Cell, July 8, 2010 DOI: 10.1016/j.cell.2010.06.018