Stress and Trauma Inhibit Uptake of Glutamic Acid in RatCerebral Cortex Slices

摘要

Glutamic acid (Glu), the most abundant amino acid in the mammalian brain, plays multiple roles in the metabolic and functional activity of the CNS. It serves as a major excitatory neurotransmitter and is involved in a variety of neurophysiological functions, including cognition, memory, and learning, during the growth and maturation of the nervous system. Regular Glu neurotransmission, which includes transmitter release into the synaptic cleft, binding to postsynaptic receptors, and high-affinity reuptake into nerve terminals, creates balance in the extra- and intracellular concentrations of Glu, which allows a healthy neuronal and glial environment.However, the long-term presence of high extracellular Glu concentrations provokes excitotoxic effects and causes apoptotic and/or necrotic processes in neurons and surrounding glial cells. Glu-mediated neuronal cell damage and death has been described in stress- and trauma-associated neurological disorders (stroke, hypoxia, hyperglycemia, and cardiac arrest), and in neurodegenerative diseases (amyotrophic lateral sclerosis, Alzheimer's disease, Parkinson's disease, etc.) [1,2].