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EAAT4 was downregulated due to the loss of Rheb1 in Purkinje cells; mTORC1 was downregulated and Akt (show AKT1 Proteins) was upregulated in Rheb1 cKO mice, suggesting that mTORC1 and Akt (show AKT1 Proteins) may be related to the downregulation of EAAT4; Rheb1 knockout decreased EAAT4 currents and slowed down the kinetics of AMPA (show GRIA3 Proteins) currents; Rheb1 deficiency did not affect the morphology of Purkinje cell layer and the development of Purkinje cells
Glutamate (show GRIN1 Proteins) transporters EAAT4 and EAAT5 (show SLC1A7 Proteins) are expressed in vestibular hair cells and calyx endings.
The role of EAAT4 in cortical glutamatergic transmission may be more important than previously thought.
Purkinje cell loss in the Inpp4a (show INPP4A Proteins)(wbl) mutant is due to glutamate (show GRIN1 Proteins) excitotoxicity initiated by the climbing fiber, and that Eaat4 may exert a protective effect.
abnormal expression of EAAT4, GABRA6 (show GABRA6 Proteins), Spi2 combined with lower levels of glutamate (show GRIN1 Proteins) and GABA are likely to be associated with the pathophysiology of Canavan disease.
These results demonstrate that EAAT4 is expressed in astrocytes. This astrocytic localization of neuronal EAAT4 may reveal a new function of EAAT4 in the central nervous system.
EAAT4 mRNA is expressed in the cerebellum of prion protein (show PRNP Proteins)-deficient (PrP-/-) mice presenting with cerebellar ataxia, at the levels identical to those in the cerebellum of non-ataxic PrP+/- mice
EAAT4 is present in the outer segments, a nonsynaptic region of photoreceptors, where it might provide a feedback mechanism for sensing extracellular glutamate (show GRIN1 Proteins) or serve as an outer barrier to prevent glutamate (show GRIN1 Proteins) from escaping from the retina.
The main role of EAAT4 is to remove low concentrations of glutamate (show GRIN1 Proteins) that escape from the uptake by glial transporters at late times and thus prevent the transmitter from spilling over to neighboring synapses.
This result demonstrates that GLAST (show SLC1A3 Proteins) plays a role in preventing excitotoxic cerebellar damage after ischemia in concert with EAAT4.
Lithium-sensitive GSK3ss is a powerful regulator of excitatory amino acid transporters EAAT3 (show SLC1A1 Proteins) and EAAT4.
Decreased SLC1A6 expression in neuregulin 1 (show NRG1 Proteins) risk variant may be an adaptive effect to restore glutamate (show GRIN1 Proteins) signalling in schizophrenia patients.
A twofold difference in functional EAAT4 levels is sufficient to alter signaling to Bergman glia in reporter mice.
strate-dependent gating of anion channels associated with excitatory amino acid transporter 4.
a conserved aspartate determines pore properties of anion channels associated with excitatory amino acid transporter 4 (EAAT4)
At least one susceptibility locus for schizophrenia may be located within or nearby SLC1A6.
Independent, rather than cooperative anion conductance gating significantly alters predictions of the influence that EAAT4-mediated anion currents will have on synaptic transmission at low glutamate (show GRIN1 Proteins) concentrations.
conclusion, maximal glutamate (show GRIN1 Proteins) transport modulation by SGK1 (show SGK1 Proteins) is accomplished by direct EAAT4 stimulation and to a lesser extent by inhibition of intrinsic Nedd4-2 (show NEDD4L Proteins).
Transports L-glutamate and also L- and D-aspartate. Seems to act as a symport by cotransporting sodium (By similarity).
solute carrier family 1 (high affinity aspartate/glutamate transporter), member 6
, excitatory amino acid transporter 4
, excitatory amino acid transporter SLC1A6
, excitatory amino acid transporter 4-like
, high-affinity neuronal glutamate transporter
, sodium-dependent glutamate/aspartate transporter
, solute carrier family 1 member 6
, solute carrier family 1, member 6
, high affinity aspartate/glutamate transporter
, glutamate transporter