Glutamate Brain Cell Damage

Head Trauma can Lead to Nerve Damage from Glutamate

There are billions of nerve cells throughout the brain. These nerves, which are also called neurons, send important messages that regulate everything from breathing, to doing math, to reaching for an object on a shelf.

Most people think of cells as tiny and round, but neurons are shaped a bit differently. Nerve cells have a more triangular shape with specialized cell parts called dendrites and axons.

The dendrites are fibers that bring electrical signals to the nerve cell body and the axon takes information away.

Messages travel up and down this cell body. One way to picture a nerve cell is to think of an old fashioned telephone cable between two poles. Each segment of telephone cable is the length of one nerve cell.

The cable between the two poles sends messages back and forth, and depending on where the call is going, zig-zags across a city from pole to pole, until it reaches its destination. It works in a similar manner inside the brain.

Many nerve cells are necessary for a message to be routed to the correct part of the brain and elicit the desired response. Between every nerve cell there is a microscopic gap that has to be crossed so the signal can continue on its path. The body uses highly specialized chemicals, which are called neurotransmitters, to cross that gap.

There are numerous chemical neurotransmitters in brain cells, and each neurotransmitter performs a bit differently.

This allows different types of messages to be sent along the nerve cells.


One of the most common neurotransmitters is called glutamate. Glutamate is classified as an excitatory neurotransmitter, because it has a stimulating effect. It is commonly used by the brain when learning and memory are activated.

Only minuscule amounts of glutamate need to be released by a nerve cell, for the neighboring nerve cell to be stimulated. However, each nerve cell has a vast store of glutamate ready, so it always has enough neurochemical available when necessary.

When a signal travels down a nerve cell, the cell releases just enough neurotransmitter to cross the gap and set of a reaction in the next nerve cell, causing the message to continue on its path.

The neurotransmitter glutamate is a powerful chemical, and in large quantities it can be toxic. Therefore, as soon as the neurotransmitter has caused its desired effect, the chemical is reabsorbed by the cell.

Glutamate and Brain Injury

When head trauma happens, nerve cells inside the brain can be stretched, torn, crushed, and split in half. Nerve cells can even be suffocated, if blood and oxygen flow are interrupted. When a nerve cell is damaged or dies, its store of chemical neurotransmitters spills out.

As the neurons release these chemicals, an immediate reaction is set off in the surrounding cells.

Since glutamate causes an excitatory response, this massive influx of neurochemical profoundly overstimulates the nerve cells in the area.

This over-stimulation causes the cells to become imbalanced. They experience an overdose of glutamate at the cellular level, and begin to die.

As cells die, more chemical neurotransmitters are released into the space between the cells, causing further cell death. There is a chain reaction that can last from hours to several days depending on the severity of the initial brain injury and other factors.


There are several head trauma treatments, including medications, which may be administered to stop the cascade of events that takes place after a traumatic brain injury with the hope of decreasing glutamate-related damage of brain cells. The biggest challenge in these cases is that circulation in the brain is often impaired due to brain swelling. When the brain is swollen inside the bony skull, this causes an increase in pressure which in turn slows blood flow.

Even if medications are provided directly into the blood stream, they have difficulty reaching the areas that need to be treated. If high brain pressure interferes with treatment, surgeons may elect to perform a craniectomy to relieve pressure.


Hinzman, J. M., Thomas, T. C., Burmeister, J. J., Quintero, J. E., Huettl, P., Pomerleau, F., & ... Lifshitz, J. (2010). Diffuse brain injury elevates tonic glutamate levels and potassium-evoked glutamate release in discrete brain regions at two days post-injury: an enzyme-based microelectrode array study. Journal Of Neurotrauma, 27(5), 889-899. doi:10.1089/neu.2009.1238

Prasad, K. N., & Bondy, S. C. (2015). Review: Common biochemical defects linkage between post-traumatic stress disorders, mild traumatic brain injury (TBI) and penetrating TBI. Brain Research, 1599103-114. doi:10.1016/j.brainres.2014.12.038

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