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Last update 08 May 2025

EAAT1

Last update 08 May 2025

Basic Info

Synonyms

EA6, EAAT1, Excitatory amino acid transporter 1

+ [8]

Introduction

Sodium-dependent, high-affinity amino acid transporter that mediates the uptake of L-glutamate and also L-aspartate and D-aspartate (PubMed:20477940, PubMed:26690923, PubMed:28032905, PubMed:28424515, PubMed:7521911, PubMed:8123008). Functions as a symporter that transports one amino acid molecule together with two or three Na(+) ions and one proton, in parallel with the counter-transport of one K(+) ion (PubMed:20477940). Mediates Cl(-) flux that is not coupled to amino acid transport; this avoids the accumulation of negative charges due to aspartate and Na(+) symport (PubMed:20477940). Plays a redundant role in the rapid removal of released glutamate from the synaptic cleft, which is essential for terminating the postsynaptic action of glutamate (By similarity).

Drugs associated with EAAT1

GDNF

Target

EAAT1

Mechanism

EAAT1 agonists

Active Org.

Fudan University

Originator Org.-

Active Indication

Diabetic Retinopathy

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

Analogue 1o(University of Copenhagen)

Target

EAAT1

Mechanism

EAAT1 blockers

Active Org.

University of Copenhagen

Originator Org.

University of Copenhagen

Active Indication-

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

UCPH-101

Target

EAAT1

Mechanism

EAAT1 blockers

Active Org.-

Originator Org.

University of Copenhagen

Active Indication-

Inactive Indication-

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with EAAT1

100 Translational Medicine associated with EAAT1

0 Patents (Medical) associated with EAAT1

1,577

Literatures (Medical) associated with EAAT1

01 Nov 2025·Neural Regeneration Research

The sexually dimorphic expression of glutamate transporters and their implication in pain after spinal cord injury

Article

Author: Rivera, Samuel E. Ocasio ; Salgado, Iris K. ; Torrado-Tapias, Aranza I. ; Miranda, Jorge D. ; Rivera, Luis H. Pagan ; Colón-Mercado, Jennifer M. ; Bracho-Rincon, Dina P. ; Santiago, José M.

JOURNAL/nrgr/04.03/01300535-202511000-00033/figure1/v/2025-03-16T134409Z/r/image-tiff In addition to the loss of motor function, ~60% of patients develop pain after spinal cord injury. The cellular-molecular mechanisms are not well understood, but the data suggests that plasticity within the rostral, epicenter, and caudal penumbra of the injury site initiates a cellular-molecular interplay that acts as a rewiring mechanism leading to central neuropathic pain. Sprouting can lead to the formation of new connections triggering abnormal sensory transmission. The excitatory glutamate transporters are responsible for the reuptake of extracellular glutamate which makes them a critical target to prevent neuronal hyperexcitability and excitotoxicity. Our previous studies showed a sexually dimorphic therapeutic window for spinal cord injury after treatment with the selective estrogen receptor modulator tamoxifen. In this study, we investigated the anti-allodynic effects of tamoxifen in male and female rats with spinal cord injury. We hypothesized that tamoxifen exerts anti-allodynic effects by increasing the expression of glutamate transporters, leading to reduced hyperexcitability of the secondary neuron or by decreasing aberrant sprouting. Male and female rats received a moderate contusion to the thoracic spinal cord followed by subcutaneous slow-release treatment of tamoxifen or matrix pellets as a control (placebo). We used von Frey monofilaments and the “up-down method” to evaluate mechanical allodynia. Tamoxifen treatment decreased allodynia only in female rats with spinal cord injury revealing a sex-dependent effect. The expression profile of glutamatergic transporters (excitatory amino acid transporter 1/glutamate aspartate transporter and excitatory amino acid transporter 2/glutamate transporter-1) revealed a sexual dimorphism in the rostral, epicenter, and caudal areas of the spinal cord with a pattern of expression primarily on astrocytes. Female rodents showed a significantly higher level of excitatory amino acid transporter-1 expression while male rodents showed increased excitatory amino acid transporter-2 expression compared with female rodents. Analyses of peptidergic (calcitonin gene-related peptide-α) and non-peptidergic (isolectin B4) fibers outgrowth in the dorsal horn after spinal cord injury showed an increased calcitonin gene-related peptide-α/ isolectin B4 ratio in comparison with sham, suggesting increased receptive fields in the dorsal horn. Although the behavioral assay shows decreased allodynia in tamoxifen-treated female rats, this was not associated with overexpression of glutamate transporters or alterations in the dorsal horn laminae fibers at 28 days post-injury. Our findings provide new evidence of the sexually dimorphic expression of glutamate transporters in the spinal cord. The dimorphic expression revealed in this study provides a therapeutic opportunity for treating chronic pain, an area with a critical need for treatment.

01 Jun 2025·Molecular and Cellular Neuroscience

Interrogating mediators of single-cell transcriptional changes in the acute damaged cerebral cortex: Insights into endothelial-astrocyte interactions

Article

Author: Theus, Michelle H ; Soliman, Eman ; de Jager, Caroline

Traumatic brain injury (TBI) induces complex cellular and molecular changes, challenging recovery and therapeutic development. Although molecular pathways have been implicated in TBI pathology, the cellular specificity of these mechanisms remains underexplored. Here, we investigate the role of endothelial cell (EC) EphA4, a receptor tyrosine kinase receptor involved in axonal guidance, in modulating cell-specific transcriptomic changes within the damaged cerebral cortex. Utilizing single-cell RNA sequencing (scRNA-seq) in an experimental TBI model, we mapped transcriptional changes across various cell types, with a focus on astrocytes and ECs. Our analysis reveals that EC-specific knockout (KO) of EphA4 triggers significant alterations in astrocyte gene expression and shifts predominate subclusters. We identified six distinct astrocyte clusters (C0-C5) in the damaged cortex including as C0-Mobp/Plp1+; C1-Slc1a3/Clu+; C2-Hbb-bs/Hba-a1/Ndrg2+; C3-GFAP/Lcn2+; C4-Gli3/Mertk+, and C5-Cox8a+. We validate a new Sox9+ cluster expressing Mertk and Gas, which mediates efferocytosis to facilitate apoptotic cell clearance and anti-inflammatory responses. Transcriptomic and CellChat analyses of EC-KO cells highlights upregulation of neuroprotective pathways, including increased amyloid precursor protein (APP) and Gas6. Key pathways predicted to be modulated in astrocytes from EC-KO mice include oxidative phosphorylation and FOXO signaling, mitochondrial dysfunction and ephrin B signaling. Concurrently, metabolic and signaling pathways in endothelial cells-such as ceramide and sphingosine phosphate metabolism and NGF-stimulated transcription-indicate an adaptive response to a metabolically demanding post-injury hypoxic environment. These findings elucidate potential interplay between astrocytic and endothelial responses as well as transcriptional networks underlying cortical tissue damage.

01 May 2025·International Journal of Biological Macromolecules

An excitatory amino acid transporter 1 acts as a novel glutamine transporter and immune modulator in the oyster Crassostrea gigas

Article

Author: Li, Deliang ; Wang, Lingling ; Yang, Chuanyan ; Ren, Wenjing ; Zhang, Xueshu ; Si, Yiran ; Song, Linsheng

Glutamine (Gln) plays a pivotal role in immunoregulation in vertebrates through transporter-mediated transport, whereas mechanisms in invertebrates remain largely unexplored. In this study, an excitatory amino acid transporter 1 (designated CgEAAT1) was identified from the Pacific oyster Crassostrea gigas, which is capable of transporting both Gln and glutamate (Glu), a functional characteristic distinct from vertebrate EAAT1 homologs. CgEAAT1 harbors a conserved Gltp domain and exhibits structural homology with vertebrate SLC1A5. Gln incubation significantly elevated CgEAAT1 and CgIL17-1 expression in hemocytes, concomitant with increased granulocyte proportions. Silencing of CgEAAT1 led to a substantial decrease in intracellular Gln levels, CgIL17-1 expression, and granulocyte proportion. Fluorescence-based assays confirmed attenuated Gln uptake following CgEAAT1 knockdown. Inhibition of CgEAAT1 expression and activity induced significant reductions in intracellular Gln concentrations and CgIL17-1 transcript levels within 6 h, with effects attenuating by 12 h, indicating complex Gln transport mechanisms in oysters. Exogenous Gln supplementation resulted in lowered larval mortality following Vibrio splendidus challenge, whereas CgEAAT1 inhibition increased mortality. These findings demonstrate that CgEAAT1 regulates hemocyte immune function through Gln transport, enhancing pathogen resistance via promotion of IL17-1 expression and granulocyte production. This research provides novel insights into Gln transport and immune regulatory mechanisms underlying molluscan environmental adaptation.

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EAAT1

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