Glutamate Transport and Preterm Brain Injury

Glutamate Transport and Preterm Brain Injury Silvia Pregnolato1*, Elavazhagan Chakkarapani1, Anthony R. Isles2 and Karen Luyt1 1Department of Neonatal Neurology, Translational Health Sciences, Bristol Medical School, University of Bristol, Bristol, United Kingdom 2Behavioural Genetics Group, MRC Centre for Neuropsychiatric Genetics and Genomics, School of Medicine, Cardiff University, Cardiff, United Kingdom Preterm birth complications are the leading cause of child death worldwide and a top global health priority. Among the survivors, the risk of life-long disabilities is high, including cerebral palsy and impairment of movement, cognition, and behavior. Understanding the molecular mechanisms of preterm brain injuries is at the core of future healthcare improvements. Glutamate excitotoxicity is a key mechanism in preterm brain injury, whereby the accumulation of extracellular glutamate damages the delicate immature oligodendrocytes and neurons, leading to the typical patterns of injury seen in the periventricular white matter. Glutamate excitotoxicity is thought to be induced by an interaction between environmental triggers of injury in the perinatal period, particularly cerebral hypoxia-ischemia and infection/inflammation, and developmental and genetic vulnerabilities. To avoid extracellular build-up of glutamate, the brain relies on rapid uptake by sodium-dependent glutamate transporters. Astrocytic excitatory amino acid transporter 2 (EAAT2) is responsible for up...
Source: Frontiers in Physiology - Category: Physiology Source Type: research

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