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Titlebook: Glial Amino Acid Transporters; Arturo Ortega,Arne Schousboe Book 2017 Springer International Publishing AG 2017 Amino Acid Transporters.GA

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Revised Ion/Substrate Coupling Stoichiometry of GABA Transporters,orters (SLC6A1, SLC6A11, SLC6A12, SLC6A13) and how the revised stoichiometry impacts our understanding of the contribution of GABA transporters to GABA homeostasis in synaptic and extrasynaptic regions in the brain under physiological and pathophysiological states. Recently, our laboratory probed th
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EAAT2 and the Molecular Signature of Amyotrophic Lateral Sclerosis,ely heterogeneous disease in both cause and symptom development, and its mechanisms of pathogenesis remain largely unknown. Excitotoxicity, a process caused by excessive glutamate signaling, is believed to play a substantial role, however. Excessive glutamate release, changes in postsynaptic glutama
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Glial GABA Transporters as Modulators of Inhibitory Signalling in Epilepsy and Stroke, through pharmacological intervention with extrasynaptic GABA. receptors that sense ambient GABA and mediate a persistent GABAergic conductance. An increase in tonic inhibition may, however, also be obtained indirectly by inhibiting glial GABA transporters (GATs). These are sodium-coupled membrane t
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Glutamate Transport System as a Novel Therapeutic Target in Chronic Pain: Molecular Mechanisms and a chemical transmitter of excitation. High-affinity glutamate transporter subtypes GLAST/EAAT1, GLT1/EAAT2, EAAC1/EAAT3, and EAAT4, differentially expressed on sensory neurons, postsynaptic spinal interneurons, and neighboring glia, ensure fine modulation of glutamate neurotransmission in the spina
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Glial Excitatory Amino Acid Transporters and Glucose Incorporation,manner, astrocytes preserve the signaling functions mediated by glutamate on synapses and prevent excitotoxicity. Additionally, EAAT activation stimulates glucose utilization in astrocytes, linking neuronal activity with astrocyte metabolism. In this chapter, we briefly review the characteristics of
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