Researchers at the Universit de Montreal (UdeM) and the Montreal Neurological Institute (MNI), McGill University have discovered that cells which normally support nerve cell (neuron) survival also play an active and major role in the death of neurons in the eye. The findings, published this week in The Journal of Neuroscience, may lead to more streamlined therapies for a variety of acute and chronic neurological disorders, including glaucoma and retinal artery occlusion.
In many neurodegenerative diseases, a main factor that kills neurons is excessive levels of glutamate, the most abundant excitatory neurotransmitter in many regions of the central nervous system (CNS). Diseases that occur as a result of high glutamate levels include hypoxicischemic brain injury (stroke), trauma, seizures, various forms of dementia and neurodegeneration. For years, the main explanation for the toxic effects of glutamate is that it overexcites neuronal cells via activation of glutamate receptors and thereby kills them.
"The most interesting aspect of our study and the reason we are so excited is that the pathway leading to glutamate-induced nerve cell death involves another vital player namely, glial cells," says Dr. Adriana Di Polo, neuroscientist at the UdeM. "Through careful experimentation we now know that glutamate activates signaling pathways in glial cells that then lead to neuronal death."
Glial cells are the most abundant cell type in the nervous system and are traditionally thought of as 'partner' cells to nerve cells providing support, nutrients and an optimal environment. However, this study indicates that glial cells also have a more sinister side that allows them to induce or exacerbate neuronal death in pathological conditions.
"Neuronal cell death induced by glutamate is a key step in a large number of injury and disease settings and this study is important because it provides a road-map for the cellular and molecu
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