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International Conference on Neurological Disorders & Stroke and Neurooncology

Dubai, UAE

Tahani Huria

Tahani Huria

Pharmacist and university lecturer-Faculty of medicine

Title: Expression of glutamate transporters (EAAC1, GLAST, GLT-1) in neonatal white matter and their role in ischaemic injury

Biography

Biography: Tahani Huria

Abstract

Neural cell death during cerebral ischaemia in neonates correlates with various significant pathological conditions, such as cerebral palsy in humans. Central white matter experiences irreversible injury when exposed to oxygen and glucose deprivation (OGD), a practical model of ischaemia. We collected evidence to examine that glutamate transporters have an essential role to perinatal white matter ischaemic injury. Several studies demonstrated that glutamate transport by oligodendrocytes maintains glutamate homeostasis in developing neonatal cerebral white matter. During ischaemia, functional activity of glutamate transporters may fail, leading to a lethal accumulation of glutamate.  Failures of glutamate transporters are responsible for excitotoxic cell injury during ischaemia with subsequent damage of white matter regions such as axons and glia. Our paper work aimed at demonstration of use of immunohistochemistry technique and examined the sub-cellular distribution of excitatory aspartate amino acid transporter (EAAC1), Glutamate–aspartate transporter (GLAST) and glutamate transporter (GLT1) proteins in the perinatal white matter using double labelling. The method using is: Immunohistochemistry technique and exposure of the optic rat nerves after dissection (RONs) to a practical model of ischaemia (OGD). The result demonstrated extensive expression of GLAST and GLT1 on the perinatal astrocyte processes while minor levels of EAAC1 expression were observed.  Although neurofilament-heavy (NF-H) axons express moderate levels of GLT1 & EAAC1 transporter proteins but they did not express GLAST transporter protein. The moderate levels of D-Aspartate uptake at NF-H and astrocyte processes confirmed the presence of functional Na+-dependent glutamate transporters. The expression of GLAST demonstrates the potential for transport mediated-glutamate release into the extracellular space result in necrosis of ischaemic white matter during the perinatal period. We have shown that high levels of glutamate transporter expression in NF-H +axons and astrocytes are consistent with a tight maintenance of extracellular glutamate in the zone where axons and glia meet. This work is consistent with several recent studies have revealed rapid astrocyte swelling will liberate astrocyte glutamate into the extracellular space in a glutamate dependent manner usually via GLAST and GLT1 transport result in necrosis of neonatal ischemic white matter. Understanding the pathophysiology in immature white matter will progressively lead scientists toward the further development of effective therapeutic interventions in the future.