Relationship between increase in astrocytic GLT-1 glutamate transport and late-LTP
Open accessAbstract
Na+-dependent high-affinity glutamate transporters have important roles in the maintenance of basal levels of glutamate and clearance of glutamate during synaptic transmission. Interestingly, several studies have shown that basal glutamate transport displays plasticity. Glutamate uptake increases in hippocampal slices during early long-term potentiation (E-LTP) and late long-term potentiation (L-LTP). Four issues were addressed in this research: Which glutamate transporter is responsible for the increase in glutamate uptake during L-LTP? In what cell type in the hippocampus does the increase in glutamate uptake occur? Does a single type of cell contain all the mechanisms to respond to an induction stimulus with a change in glutamate uptake? What role does the increase in glutamate uptake play during L-LTP? We have confirmed that GLT-1 is responsible for the increase in glutamate uptake during L-LTP. Also, we found that astrocytes were responsible for much, if not all, of the increase in glutamate uptake in hippocampal slices during L-LTP. Additionally, we found that cultured astrocytes alone were able to respond to an induction stimulus with an increase in glutamate uptake. Inhibition of basal glutamate uptake did not affect the induction of L-LTP, but inhibition of the increase in glutamate uptake did inhibit both the expression of L-LTP and induction of additional LTP. It seems likely that heightened glutamate transport plays an ongoing role in the ability of hippocampal circuitry to code and store information.
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Pathological tau impairs astrocyte-mediated glutamate transport, resulting in pathological glutamate accumulation and excitotoxicity.
“In addition, pathological tau may impair astrocyte-mediated glutamate transport, resulting in pathological glutamate accumulation in the brain and the consequent excitotoxicity [438, 439].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [438]
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Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease
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- Authors
- Pita-Almenar, J. D., Zou, S., Colbert, C. M., & Eskin, A.
- Affiliations
- University of Houston (US)
- Venue
- Learning & Memory
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-11-19
- Volume
- 19
- Issue
- 12
- Pages
- 615-626
- ISSN
- 1072-0502 (ISSN-L)
- 1549-5485
- PMC
- PMC3506973
- OpenAlex
- W2108370047
- Cited by
- 52
- References
- 58
- Citations by year
- 2025: 2 · 2024: 2 · 2023: 3 · 2022: 2 · 2021: 8 · 2020: 2 · 2019: 5 · 2018: 2 · 2017: 4 · 2016: 5 · 2015: 9 · 2014: 6 · 2013: 2
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Learning & Memory (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- National Institutes of Health
- National Institute of Neurological Disorders and Stroke (NS28462, R01NS028462)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Biochemistry › Amino Acid Enzymes and Metabolism
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Keywords
- GLT-1, glutamate transporters, astrocytes, glutamate uptake, hippocampus, synaptic plasticity, glutamate clearance, LTP induction, astrocyte plasticity
- MeSH terms
- Alanine Transaminase, Analysis of Variance, Animals, Animals, Newborn, Aspartic Acid, Astrocytes, Biophysics, Cells, Cultured, Electric Stimulation, Flow Cytometry, Colforsin, Glial Fibrillary Acidic Protein, Glutamates, Glycine, Hippocampus, Indoles, Kainic Acid, Male, Neurons, Quinoxalines, Tetrodotoxin, Valine, Rats, Sprague-Dawley, Long-Term Potentiation, Excitatory Amino Acid Agonists, Excitatory Amino Acid Antagonists, Glutamic Acid, Excitatory Postsynaptic Potentials, Biotinylation, Protein Transport, Sodium Channel Blockers, Excitatory Amino Acid Transporter 1, Excitatory Amino Acid Transporter 2, Rats, In Vitro Techniques
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