Slc1A3 Gene is an important component in the neurobiology of neurodegenerative diseases. This page provides detailed information about its structure, function, and role in disease processes.
SLC1A3 (Solute Carrier Family 1 Member 3), also known as EAAT1 (Excitatory Amino Acid Transporter 1) or GLAST (Glutamate Aspartate Transporter), is a gene that encodes a high-affinity glutamate transporter protein. This transporter is primarily expressed in astrocytes and plays a critical role in maintaining extracellular glutamate homeostasis in the central nervous system by clearing glutamate from the synaptic cleft after neurotransmission[1][2].
| Property | Value |
|---|---|
| Gene Symbol | SLC1A3 |
| Full Name | Solute Carrier Family 1 Member 3 |
| Previous Names | EAAT1, GLAST |
| Chromosomal Location | 5p13.2 |
| NCBI Gene ID | 6507 |
| OMIM | 600116 |
| Ensembl ID | ENSG00000081189 |
| UniProt ID | P43003 |
The SLC1A3-encoded protein is a transmembrane protein with several key structural features:
The transporter operates as a trimer, with each monomer capable of transporting glutamate independently. The binding site accommodates both L-glutamate and L-aspartate with high affinity.
SLC1A3/EAAT1 is the primary glutamate transporter in the cerebellum and is also expressed throughout the brain:
| Brain Region | Expression Level |
|---|---|
| Cerebellum | Highest (Bergmann glia) |
| Hippocampus | Moderate (astrocytes) |
| Cerebral Cortex | Moderate |
| Brainstem | Low-Moderate |
| Spinal Cord | Moderate |
SLC1A3 mutations cause episodic ataxia type 6, characterized by:
[1] Shanker, G. et al. (2001). Expression and function of glutamate transporters in astrocytes. Neurochemical Research, 26(4), 357-365.
[2] Robinson, M.B. (1998). The family of sodium-dependent glutamate transporters. Neurochemistry International, 33(6), 479-491.
[3] Jen, J.C. et al. (2005). Mutations in SLC1A3 cause episodic ataxia type 6. Brain, 128(Pt 8), 1868-1876.
[4] Masliah, E. et al. (1996). Patterns of glutamate transporter expression in the frontal cortex in Alzheimer's disease. Brain Research, 722(1-2), 160-174.
The study of Slc1A3 Gene has evolved significantly over the past decades. Research in this area has revealed important insights into the underlying mechanisms of neurodegeneration and continues to drive therapeutic development.
Historical context and key discoveries in this field have shaped our current understanding and will continue to guide future research directions.
[1] Shanker G, et al. Expression and function of glutamate transporters in astrocytes. Neurochemical Research. 2001;26(4):357-365.
[2] Robinson MB. The family of sodium-dependent glutamate transporters. Neurochemistry International. 1998;33(6):479-491.
[3] Jen JC, et al. Mutations in SLC1A3 cause episodic ataxia type 6. Brain. 2005;128(Pt 8):1868-1876.
[4] Masliah E, et al. Patterns of glutamate transporter expression in the frontal cortex in Alzheimer's disease. Brain Research. 1996;722(1-2):160-174.
[5] Rothstein JD, et al. Localization of neuronal and glial glutamate transporters. Neuron. 1994;13(3):713-725.
Note: This page is part of the NeuroWiki gene database. Last updated: 2026-03-04