When we exercise our muscles produce lactate, a waste product of glucose metabolism, in both the muscles and the brain. A team of researchers from EFPL in Switzerland and the King Abdullah University of Science and Technology has found that lactate is able to protect neurons from damage when they’ve suffered acute trauma, such as stroke or injury to the spinal cord.
During trauma, the nerve cells receive excessive stimulation, leading to damage and ultimately death, a process known as excitotoxicity. It’s one of the reasons why receiving medical attention quickly after such trauma is so important. This damage is also implicated in progressive neurodegenerative diseases, such as Alzheimer’s. Now scientists have discovered that lactate can offer a protective effect against this damage.
When we suffer acute trauma to the brain, specific receptors known as NMDA receptors, which interact with glutamate, become extremely active, overwhelming the target neuron with electrical signals and causing calcium ions to build up inside the cell. This build-up then triggers toxic biochemicals that can go on to damage or kill the cell.
Researchers investigate effect of glutamate using a non-invasive imaging technique
The researchers chose to investigate the effects of glutamate on cultured mice brain neurons, using a novel, non-invasive imaging technique that can visualise the structure of the cells with extremely high resolution. Although previous studies have indicated that lactate may have the potential to protect neurons from excitotoxicity, the reason why has proved extremely elusive until now. In order to test their theory, the team tested the effects that glutamate on the cultured mouse neurons, both with and without lactate. They found that the glutamate killed 65% of the neurons without lactate, but just 32% of the neurons with lactate.
Following this discovery, the team wanted to find out how lactate protects the neurons. They did this by utilising different receptor blockers on the mouse neurons, which showed that lactate triggers ATP production, the energy molecule within the cell. This ATP was then seen to bind and turn on a different receptor within the neuron, which then activated an intricate series of defence mechanisms. This resulted in the neuron being able to resist the assault of signals from the NMDA receptor.
The findings from this study are exciting as they offer an insight into neuroprotection, which could lead to new treatments for the currently irreversible damage caused by stroke, injuries to the spinal cord and other such traumas.
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