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A Drosophila tripartite synapse model which exhibits morphological and functional properties similar to those of mammalian synapses.
Eaat1 expression is promoted by Fringe-mediated neuron-glial communication during development and suggest that Eaat1 plays an essential role in regulating central nervous system neural circuits that control locomotion in Drosophila
Terminal glial differentiation involves regulated expression of the excitatory amino acid transporters in the Drosophila embryonic CNS.
dEAAT1 is present at the adult, but surprisingly not at embryonic and larval NMJ, suggesting a physiological maturation of the junction during metamorphosis
EAAT1 rs2731880 SNP is associated with amygdala functional connectivity in bipolar disorder.
Episodic ataxias 6 is caused by heterozygous mutations in SLC1A3, which encodes a subunit of a glial excitatory amino acid transporter, EAAT1.
a novel missense mutation, c.383T>G (p.Met128Arg) in SLC1A3, in an episodic ataxia patient by whole-exome sequencing.
This is the first study to link SLC1A3 and EPHB2 to clinically relevant vertebral osteoporosis phenotypes.
crystal structures of a thermostabilized human SLC1 transporter, the excitatory amino acid transporter 1 (EAAT1), with and without allosteric and competitive inhibitors bound
This study demonstrated that the cytopathology and episodic paralysis in our Drosophila EA6 model stem from a gain-of-function chloride channelopathy of glial cells..
Starvation of Muller cells increased the glutamate uptake capacity as well as the expression of the most abundant glutamate transporter, EAAT1.
A heterozygous SLC1A3 c.1177G4A mutation has been detected in a patient with late-onset episodic ataxia. Same heterozygous mutation was identified in one clinically affected family member and two asymptomatic members.
that Abeta1-42 oligomers could cause disturbances in insulin/Akt/EAAT signaling in astrocytes
We consider an association between SLC1A3 and the behavioural problems which can also be considered a contributing factor to behavioural problems in larger duplications overlapping the 5p13 microduplication syndrome region.
In combination with other nearby residues, Arg-388 coordinates anion channel gating and forms part of the missing structural link between the anion conducting and substrate transport states in EAAT1.
SPAK and OSR1 are powerful negative regulators of the excitatory glutamate transporters EAAT1 and EAAT2.
There was no association between pyramidal cell EAAT1 splice variant expression and schizophrenia.
data provide additional insights into the mechanism by which substrates gate the anion conductance in EAATs and suggest that in EAAT1, Arg-388 is a critical element for the structural coupling between the substrate translocation and the gating mechanisms
discovering compounds that can enhance EAAT1 expression and activity may be a novel strategy for therapeutic treatment of glaucoma.
Results showed that EAAT2 levels were significantly decreased in the essential tremor cerebellar cortex, in contrast to similar levels of EAAT1 levels between essential tremor cases and controls
EAAT1 polymorphism which is involved in the Regulation of extracellular glutamate concentrations, influences Cognitive performances with a detrimental effect of T/T homozygosis.
the delivered miR-124 increased the expression of the glutamate transporters, EAAT1 in NPCs and EAAT2 in both NPCs and astrocytes.
Results describe EAAT1 and EAAT2 labeling in the prefrontal cortex in human postmortem control brains at the light and electron microscopic level
Its dysregulation may contribute to the pathology and possibly affect the onset of fragile X-associated tremor/ataxia syndrome.
Study shows that high-fat feeding induces metabolic disorders and disrupts lactate metabolism in the hippocampus. Glial glutamate transporters GLAST and GLT-1 may contribute to the high-fat diet induced abnormalities of the hippocampal lactate metabolism.
glutamate transporter function by GLAST on Bergmann glia plays important roles in development and maintenance of proper synaptic wiring and wrapping in Purkinje cells
Loss of EAAT4 accounts for the initial hyper-excitability of Purkinje cells lacking b-III spectrin and that loss of GLAST appears to work synergistically to worsen motor deficits. When levels of both EAAT4 and GLAST are compromised in b-III(-/-) mice, the proximal dendrites of Purkinje cells within the posterior cerebellum are the most vulnerable to degeneration.
The results of this study concluded that EAAT anion channels play an important and unexpected role in adjusting glial intracellular anion concentration during maturation and in response to cerebellar activity.
SLC1A3 maintains a constant import of acidic amino acids independently of nutritional status in adipocytes.
glutamate/aspartate transporter (GLAST) was elevated in 8- to 10- and/or 20- to 22-month GHR-KO mice when comparing genotypes
This study findings demonstrate that Ascl1(CreERT2) and Glast(CreERT2) mouse lines enable simple and reliable labeling of adult-born GC lineages within restricted time windows.
arundic acid treatment prevented RGC death by upregulating GLAST in heterozygous (GLAST(+/-)) mice
Results show that expression of GLAST is decreased in cerebellar astrocytes in a mouse model of SCA1; decrease occurs in non-cell autonomous manner late in disease and correlates well with the loss of Purkinje neurons
we have demonstrated for the first time that DOR receptor activation induces astrocytic expression of EAAT1 and EAAT2
The result showed significant correlation between changes in GLUT 8 and glucose levels with changes in StAR level in the testis and circulating testosterone level in the mice from birth to senescence
EAAT1 activity and sodium potassium-ATPase activity are co-regulated by a tightly coupled homeostatic relationship in astrocytes.
Study suggests that there is a remarkable subcellular heterogeneity of GLAST and GLT-1 expression in the developing hippocampus
TNR is expressed in a subset of astrocytes and contributes to glutamate homeostasis by regulating astrocytic GLAST expression.
Results suggest that an impairment of astrocytic ascorbate-release may exacerbate neuronal dysfunction in neurodegenerative disorders and acute brain injury in which excitotoxicity and/or GLAST deregulation have been implicated.
deletion appeared to preferentially affect the maintenance of a normal postsynaptic/neuronal phenotype, evident only with increasing age
These findings demonstrate that GltI and Glast negatively regulate calcium-dependent proliferation in vitro and that their upregulation after injury is associated with decreased proliferation after brain trauma.
BDNF can up-regulate GLAST and GS and increase glutamate uptake during hypoxia, and these functions may underlie its neuroprotective effects.
Together, these studies strongly suggest that NF-kappaB contributes to neuron-dependent regulation of astrocytic GLT-1 transcription.
Glutamate substrate increases GLAST activity and up-regulates the expression of GLAST protein in retinal Muller cells.
This gene encodes a member of a member of a high affinity glutamate transporter family. Mutations in this gene are associated with episodic ataxia, Type 6. Alternative splicing results in multiple transcript variants.
, drosophila glutamate transporter-1
, excitatory amino acid transporter 1
, glutamate transporter
, sodium-dependent excitatory amino acid transporter 1
, sodium-dependent glutamate transporter
, excitatory amino acid transporter SLC1A3a
, solute carrier family 1 (glial high affinity glutamate transporter), member 3
, Na+-dependent glutamate/aspartate transporter
, Sodium-dependent glutamate/aspartate transporter 1
, excitatory amino acid transporter 1-like
, glial glutamate transporter
, glutamate/aspartate transporter
, sodium-dependent glutamate/aspartate transporter 1
, solute carrier family 1, member 3
, solute carrier family 1 member 3
, glial high affinity glutamate transporter
, high-affinity neuronal glutamate transporter