Glutamate, the primary excitatory neurotransmitter in the CNS, is regulated by the excitatory amino acid transporters (EAATs) GLT-1 and GLAST. Following traumatic brain injury (TBI), extracellular glutamate levels increase, contributing to excitotoxicity, circuit dysfunction, and morbidity. Increased neuronal glutamate release and compromised astrocyte-mediated uptake contribute to elevated glutamate, but the mechanistic and spatiotemporal underpinnings of these changes are not well established.
View Article and Find Full Text PDFAstrocytes are glial cells that interact with neuronal synapses via their distal processes, where they remove glutamate and potassium (K) from the extracellular space following neuronal activity. Astrocyte clearance of both glutamate and K is voltage dependent, but astrocyte membrane potential (V) is thought to be largely invariant. As a result, these voltage dependencies have not been considered relevant to astrocyte function.
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