The DOI matches its Crossref record; 235 of the 235 references it cites were found in a registry or an index.
The role of astrocytic glutamate transporters GLT-1 and GLAST in neurological disorders: Potential targets for neurotherapeutics
Open accessAbstract
Glutamate is the primary excitatory neurotransmitter in the central nervous system (CNS) that initiates a rapid signal transmission in the synapse before its re-uptake into the surrounding glia, specifically astrocytes. The astrocytic glutamate transporters, glutamate-aspartate transporter (GLAST) and glutamate transporter-1 (GLT-1) and their human homologs excitatory amino acid transporter 1 (EAAT1) and 2 (EAAT2), respectively, are the major transporters that take up synaptic glutamate to maintain its optimal extracellular levels, thus preventing its accumulation in the synaptic cleft and the ensuing excitotoxicity. Growing evidence has shown that excitotoxicity is associated with various neurological disorders, including amyotrophic lateral sclerosis (ALS), Alzheimer’s disease (AD), Parkinson’s disease (PD), manganism, ischemia, schizophrenia, epilepsy, and autism. While the mechanisms of neurological disorders are not well understood, the dysregulation of GLAST/GLT-1 may play a significant role in excitotoxicity and associated neuropathogenesis. The expression and function of GLAST/GLT-1 may be dysregulated at the genetic, epigenetic, transcriptional or translational levels, leading to high levels of extracellular glutamate and excitotoxicity. Consequently, understanding the regulatory mechanisms of GLAST/GLT-1 has been an area of interest in developing therapeutics for the treatment of neurological disorders. Pharmacological agents including β-lactam antibiotics, estrogen/selective estrogen receptor modulators (SERMs), growth factors, histone deacetylase inhibitors (HDACi), and translational activators have shown significant efficacy in enhancing the expression and function of GLAST/GLT-1 and glutamate uptake in both in vitro and in vivo settings. This comprehensive review will discuss the regulatory mechanisms of GLAST/GLT-1, their association with neurological disorders, and the pharmacological agents that mediate their expression and function.
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Cited by
Mead, R. J., Shan, N., Reiser, H. J., Marshall, F., & Shaw, P. J. (2023) · Nature Reviews Drug Discovery · doi:10.1038/s41573-022-00612-2 · Cited by 505
Astrocyte contribution to dysfunction, risk and progression in neurodegenerative disorders
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Revisiting the role of neurotransmitters in epilepsy: An updated review
Akyuz, E., Polat, A. K., Eroglu, E., Kullu, I., Angelopoulou, E., & Paudel, Y. N. (2021) · Life Sciences · doi:10.1016/j.lfs.2020.118826 · Cited by 303
Blood–Brain Barrier Breakdown in Alzheimer’s Disease: Mechanisms and Targeted Strategies
Alkhalifa, A. E., Al-Ghraiybah, N. F., Odum, J., Shunnarah, J. G., Austin, N., & Kaddoumi, A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms242216288 · Cited by 212
Inflammation context in Alzheimer’s disease, a relationship intricate to define
Novoa, C., Salazar, P., Cisternas, P., Gherardelli, C., Vera-Salazar, R., Zolezzi, J. M., & Inestrosa, N. C. (2022) · Biological Research · doi:10.1186/s40659-022-00404-3 · Cited by 206
Metadata
- Authors
- Pajarillo, E., Rizor, A., Lee, J., Aschner, M., & Lee, E.
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2019-12
- Volume
- 161
- Pages
- 107559
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W2921594363
- Cited by
- 478
- References
- 235
- FWCI
- 15.89
- Type
- journal article
- Language
- en
- Open access
- green
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