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Glutamate uptake
Abstract
Brain tissue has a remarkable ability to accumulate glutamate. This ability is due to glutamate transporter proteins present in the plasma membranes of both glial cells and neurons. The transporter proteins represent the only (significant) mechanism for removal of glutamate from the extracellular fluid and their importance for the long-term maintenance of low and non-toxic concentrations of glutamate is now well documented. In addition to this simple, but essential glutamate removal role, the glutamate transporters appear to have more sophisticated functions in the modulation of neurotransmission. They may modify the time course of synaptic events, the extent and pattern of activation and desensitization of receptors outside the synaptic cleft and at neighboring synapses (intersynaptic cross-talk). Further, the glutamate transporters provide glutamate for synthesis of e.g. GABA, glutathione and protein, and for energy production. They also play roles in peripheral organs and tissues (e.g. bone, heart, intestine, kidneys, pancreas and placenta). Glutamate uptake appears to be modulated on virtually all possible levels, i.e. DNA transcription, mRNA splicing and degradation, protein synthesis and targeting, and actual amino acid transport activity and associated ion channel activities. A variety of soluble compounds (e.g. glutamate, cytokines and growth factors) influence glutamate transporter expression and activities. Neither the normal functioning of glutamatergic synapses no…
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“The astroglial cells are the main regulators of cerebral glutamate clearance and metabolism [21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [25]
In the citing paper
“which in turn can be reconverted into glutamate for use either as a neurotransmitter or energy substrate [21, 22, 23, 24, 25, 26, 27].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [25]
In the citing paper
“Through the membrane glutamate aspartate transporter (GLAST), the astroglia dynamically remove glutamate from the extracellular milieu, restricting its signaling activity in time and space and allowing for its recycling [25, 30, 33].”
From Gliovascular alterations in sporadic and familial Alzheimer's disease: APOE3 Christchurch homozygote glioprotection (2023) · cites this paper as [25]
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Metadata
- Authors
- Danbolt, N. C.
- Affiliations
- University of Oslo (NO)
- Corresponding author
- Danbolt, Niels C
- ORCID
- Danbolt, Niels C
- Venue
- Progress in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2001-09
- Volume
- 65
- Issue
- 1
- Pages
- 1-105
- ISSN
- 0301-0082 (ISSN-L)
- OpenAlex
- W4210979710
- Cited by
- 4,227
- References
- 19
- Citations by year
- 2026: 94 · 2025: 113 · 2024: 133 · 2023: 126 · 2022: 177 · 2021: 167 · 2020: 186 · 2019: 144 · 2018: 180 · 2017: 199 · 2016: 214 · 2015: 209 · 2014: 241 · 2013: 203 · 2012: 195
- FWCI
- 11.41
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Progress in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- 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 › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
- Keywords
- glutamate uptake, glutamate transporters, brain, glial cells, neurons, neurotransmission, GABA synthesis, glutathione, energy metabolism, cytokines, neurological disorders, cerebral ischemia, epilepsy, Alzheimer's disease, amyotrophic lateral sclerosis, traumatic brain injury, schizophrenia, osteoporosis
- MeSH terms
- Ethanol, Anesthetics, Animals, Bone and Bones, Brain, Carrier Proteins, Extracellular Space, Female, Gene Expression Regulation, Glutamine, Hepatic Encephalopathy, Humans, Intracellular Fluid, Ion Channels, Ischemia, Male, Mammals, Mercury Poisoning, Nerve Tissue Proteins, Nervous System Diseases, Synaptic Transmission, Neuroglia, Neurons, Organ Specificity, Placenta, Potassium, Pregnancy, Protein Conformation, Sodium, Synapses, Viscera, Ion Channel Gating, HIV Infections, Ion Transport, Receptors, Glutamate, Neurotransmitter Agents, ATP-Binding Cassette Transporters, Glutamic Acid, Amino Acid Transport System X-AG, Monocarboxylic Acid Transporters, Rats
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