HistoryThe harmful effect of glutamate upon the CNS were first observed in 1954 by T. Hayashi, a Japanese scientist who noted that direct application of glutamate to the CNS caused seizure activity, though this report went unnoticed for several years.
The toxicity of glutamate was then observed by D. R. Lucas and J. P. Newhouse in 1957, when the subcutaneous injection of monosodium glutamate to newborn mice destroyed the neurons in the inner layers of the retina.
Later, in 1969, John Olney discovered the phenomenon was not restricted to the retina, but occurred throughout the brain, and coined the term excitotoxicity. He also assessed that cell death was restricted to postsynaptic neurons, that glutamate agonists were as neurotoxic as their efficiency to activate glutamate receptors, and that glutamate antagonists could stop the neurotoxicity.
Subsequent research by Mark Mattson provided evidence for the involvement of excitotoxicity in Alzheimer's disease, and other age-related neurodegenerative conditions that involve oxidative stress and cellular energy deficits.
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