Elsevier

Molecular Brain Research

Volume 36, Issue 1, February 1996, Pages 163-168
Molecular Brain Research

Short communication
Cloning and expression of a neuronal rat brain glutamate transporter

https://doi.org/10.1016/0169-328X(95)00279-2Get rights and content

Abstract

Glutamate is the major excitatory transmitter in the mammalian central nervous system. Glutamate transporters, which keep the extracellular glutamate concentration low, are required both for normal brain function and for protecting neurons against harmful glutamatergic overstimulation. We have isolated the cDNA for a rat brain glutamate transporter (REAAC1) which has 90% amino acid and 86% nucleotide identity to the rabbit EAAC1. When REAAC1 was expressed in HeLa cells using a recombinant vaccinia-T7 virus expression system, a sodium dependent glutamate uptake was observed. The affinity of the carrier to various substrates was typical of brain ‘high affinity’ glutamate uptake: threo-3-hydroxyaspartate, (R)-aspartate, (S)-glutamate and (S)-trans-pyrrolidine-2,4-dicarboxylic acid were strong inhibitors, but not (R)-glutamate or γ-aminobutyrate. High resolution, non-radioactive in situ hybridization histochemistry in rat brain revealed the mRNA in several types of glutamatergic as well as non-glutamatergic neurons, but not in glial cells.

References (43)

Cited by (58)

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    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).

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    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.

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    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).

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