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Coupling of Glutamate Uptake and Degradation in Transmitter Clearance: Anatomical Evidence

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Neutrotransmitter Release and Uptake

Part of the book series: NATO ASI Series ((ASIH,volume 100))

Abstract

One reason for investigating glutamate uptake in the CNS has been the requirement for rather low extracellular glutamate levels (ca. 1μM) and their tight homeostatic control. Without it, raised extracellular glutamate would lead to uncontrolled neuronal excitation and, ultimately, to neuronal death. The inactivation of glutamate seems to rely both on its uptake and its subsequent enzymatic degradation because — as hypothesized below- uptake is dependent on efficient intracellular removal of glutamate. Regarding the proteins mediating these processes, four high affinity glutamate transporters have been described (Danbolt, 1994; Fairman et al., 1995) and three of them localized in the rat CNS (Rothstein et al., 1994).

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© 1997 Springer-Verlag Berlin Heidelberg

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Derouiche, A. (1997). Coupling of Glutamate Uptake and Degradation in Transmitter Clearance: Anatomical Evidence. In: Pöğün, Ş. (eds) Neutrotransmitter Release and Uptake. NATO ASI Series, vol 100. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60704-2_20

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  • DOI: https://doi.org/10.1007/978-3-642-60704-2_20

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