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Neurons may not be the superstars we think they are after all. It may be our other brain cells, the glia, the ugly ducklings of the brain, which actually have the really important role.

When you think about brain cells you would normally be thinking about neurons. These are the brain cells involved in transmitting electrical impulses between themselves, releasing a selection of over 300 neurochemicals so that we can all enjoy our thoughts, feelings and actions. We have around 85 billion of them.

But there are an equal number of other brain cells in our heads which up until recently were thought of as merely having a supporting role, providing the glue to bind our brain cells together. Indeed glia comes from the Greek word meaning “glue”. Yet our glial cells are now being revealed to be equal superstars in their own right and studies are now starting to unravel the mystery of what the true role of our glial cells may be.

Welcome to the world of glial cells.

Researchers from the Tel Aviv University have been studying glial cells and have discovered that they are central to our brain’s plasticity: the ability of our brain to form new synaptic connections between other brain cells.
One type of glial cells are called astrocytes and it is these, which appear to be involved in controlling synaptic communication.

Our brain’s plasticity enables us to learn new information, store it and adapt to changing circumstances.

Maurizio de Pitta along with other researchers from the Salk Institute, the University of California and University of Lyon have developed a computer model which incorporates the influence of the glial cells on the transfer of information at the level of the synapse.

The parts of the brain most highly involved in memory and learning are the hippocampus and the cerebral cortex. Perhaps not surprisingly these areas are abundant in glial cells as well as neurons. So much so that for every neuron in these areas there are between two to five glial cells.

So what are these glial cells doing?

The researchers believe that the glial cells work as moderators of the neurochemical information being transported at the synapses
They can either ramp things up to prompt the transfer of information or slow synaptic activity down if the synapses are overactive. The end result? The glial cells basically are orchestrating the transmission of information for optimal brain function.

They do this by “listening in” to the neurons and communicating between themselves using the same neurotransmitter receptors as neurons but without using electrical impulses.

This major difference is that whereas neurons communicate with each other serially through their multitude of synaptic connections, glia communicate more widely like radio waves and at a slower pace than the zippy neurons.

Is this relevant to better understanding certain brain diseases?

Prof Ben-Jacob notes that these findings could have important implications for a number of brain disorders such as epilepsy and neurodegenerative diseases such as Alzheimer’s.

Glial cells and epilepsy

When a person has an epileptic seizure, the activity of neurons in one location spread and take over the normal activity of other locations This is explained as the glial cells here failing to adequately regulate synaptic transmission.

In other conditions if neuronal activity is noted to be low, the glial cells act to boost transmission of information by maintaining the synaptic plasticity between brain cells.

Glial cells and Alzheimer’s

Douglas Fields asks whether in Alzheimer’s the pathology occurs as a result of a failure of the associated glia to clear waste. These specialised microglia have a particular role in destroying bacteria and by clearing away diseased tissue promoting tissue recovery and repair.

Wolfgang Streit from the University of Florida has noted that the microglia degenerate and become weaker with age. In Alzheimer’s disease much of the early neuronal loss occurs in the area of the hippocampus. Streit has demonstrated that the degeneration of microglia follows a similar pattern leading to the question of whether Alzheimer’s disease is a problem associated with ageing microglia no longer able to perform their usual function of clearing waste such as amyloid.

Glial cells and chronic pain

A number of researchers from the US, Japan and the UK have discovered that both microglia and astrocytes respond to the activity of pain circuits following injury by releasing neurochemicals to support neurons and stimulate healing. What appears to happen in some cases is that the microglia don’t turn off when the healing is complete, a bit like the never ending porridge pot, so the pain circuits continue to fire.

Glial cells and mental illness

Research into depression and schizophrenia has shown that these conditions are associated with reduced numbers of glial cells – oligodendrocytes and astrocytes. Because astrocytes are associated with regulating the amount of neurotransmitters at synapses, having lower levels of these glial cells may be a contributor to these conditions. It has been proposed that targeting these glia may provide a new method of treatment.

As this fascinating research continues to unravel the mysteries of the true function of glial cells, we may have to change our previous perspective that our brain’s super plasticity is based on neuronal activity alone. It appears that we need our glial cells to keep our neurons on task and efficient – a bit like a master coach.

Maurizio De Pittà, Vladislav Volman, Hugues Berry, Eshel Ben-Jacob. A Tale of Two Stories: Astrocyte Regulation of Synaptic Depression and Facilitation. PLoS Computational Biology, 2011; 7 (12): e1002293 DOI: 10.1371/journal.pcbi.1002293

Scientific American Mind: R. Douglas Fields The Hidden Brain May/June 2011 Pages 53 – 57

Dr Jenny Brockis

Dr Jenny Brockis is a medical practitioner and internationally board-certified lifestyle medicine physician, workplace health and wellbeing consultant, keynote speaker and best-selling author. You can now pre-order her new book ‘The Natural Advantage’ due for publication in October 2024.

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