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L-Glutamic acid is a non-essential amino acid and the primary excitatory neurotransmitter in the CNS.1 It acts on ionotropic and metabotropic receptors to induce excitatory synaptic transmission and has roles in synaptic plasticity. Excessive release of L-glutamic acid induces excitotoxicity that is associated with various human diseases, including amyotrophic lateral sclerosis (ALS), stroke, Parkinson’s disease, Alzheimer’s disease, and Huntington’s disease.2 Excessive L-glutamic acid release, in its protonated glutamate form, also occurs during seizure activity and contributes to epileptogenesis and seizure-induced brain damage.3
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1. Glutamic acid, twenty years later. J. Nutr. 130(4S Suppl), 901S-909S (2000).
2. The role of glutamate in neurotransmission and in neurologic disease. Arch. Neurol. 43(10), 1058-1063 (1986).
3. Glutamatergic mechanisms associated with seizures and epilepsy. Cold Spring Harb. Perspect. Med. 5(8), a022863 (2015).
Glutamate decreases oxidative stress and lipid droplet formation in astrocytes. J. Cell Sci. 138(19), jcs263983 (2025).