Short communicationCloning and expression of a neuronal rat brain glutamate transporter
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Cited by (58)
Novel aspects of glutamine synthetase in ammonia homeostasis: Glutamine synthetase and ammonia
2020, Neurochemistry InternationalGlutamate transporters: Gene expression regulation and signaling properties
2019, NeuropharmacologyCitation Excerpt :It is important to note that this transporter has also been found in neurons (Danbolt et al., 2016). EAAT3/EAAC1 is a neuronal transporter widely expressed in the encephalon and localized mainly to the soma and dendrites (Bjørås et al., 1996; Holmseth et al., 2012; Kanai and Hediger, 1992; Rothstein et al., 1994; Shashidharan et al., 1997). EAAT4 is predominantly found in cerebellar Purkinje cells, where it is targeted to dendrites and spines and it is also expressed in a subset of forebrain neurons (de Vivo et al., 2010; Dehnes et al., 1998; Fairman et al., 1995; Massie et al., 2008).
Neuronal vs glial glutamate uptake: Resolving the conundrum
2016, Neurochemistry InternationalCitation Excerpt :Lack of EAAT1 is thereby less dramatic than lack of EAAT2 (see above), but as the expression is not neuronal it will not be discussed further in this review. EAAT3 (Kanai and Hediger, 1992; Arriza et al., 1994; Bjørås et al., 1996) is a neuronal transporter as originally suggested and it is not expressed in glial cells (Rothstein et al., 1994; Shashidharan et al., 1997; Holmseth et al., 2012b). It appears to be expressed in most, if not all, neurons throughout the CNS.
Age-dependent modifications in the mRNA levels of the rat excitatory amino acid transporters (EAATs) at 48 hour reperfusion following global ischemia
2010, Brain ResearchCitation Excerpt :The EAAC1 response to I/R insult presented a similar pattern to that observed in GLT-1 in both 3-month-old and 18-month-old animals. As a neuronal specific transporter (Kanai and Hediger, 1992; Rothstein et al., 1994; Bjoras et al., 1996; Berger and Hediger, 1998), EAAC1 response to I/R could mirror the neuronal damage and its similarity with the GLT-1 response gives additional support to the hypothesis previously discussed that GLT-1 response to I/R is due to neuronal rather than to glial changes. It is worthy to bear in mind that neurons release the neurotransmitter glutamate, which is then uptaken by glial cells, where it is transformed into glutamine, which, in turn, diffuses through the extracellular space into neurons for the synthesis of glutamate (Segovia et al., 2001).