Insufficient glutamine synthetase activity during synaptogenesis causes spatial memory impairment in adult mice
Open accessAbstract
Glutamatergic synapses constitute a major excitatory neurotransmission system and are regulated by glutamate/glutamine (Gln) cycling between neurons and astrocytes. Gln synthetase (GS) produced by astrocytes plays an important role in maintaining the cycle. However, the significance of GS during synaptogenesis has not been clarified. GS activity and expression significantly increase from postnatal day (PD) 7 to 21, and GS is expressed prior to glial fibrillary acidic protein (GFAP) and is more abundant than GFAP throughout synaptogenesis. These observations suggest that GS plays an important role in synaptogenesis. We investigated this by inhibiting GS activity in neonatal mice and assessed the consequences in adult animals. Lower expression levels of GS and GFAP were found in the CA3 region of the hippocampus but not in the CA1 region. Moreover, synaptic puncta and glutamatergic neurotransmission were also decreased in CA3. Behaviorally, mice with inhibited GS during synaptogenesis showed spatial memory-related impairment as adults. These results suggest that postnatal GS activity is important for glutamatergic synapse development in CA3.
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Glutamine synthetase (GS) catalyzes the condensation of ammonium and glutamate into glutamine.
“Complementarily, the cytoplasmic enzyme glutamine synthetase (GS) catalyzes the condensation of ammonium and glutamate into glutamine [24, 27, 29], 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: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [27]
Astroglial cells are the main regulators of cerebral glutamate clearance and metabolism.
“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: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [27]
Glutamine can be reconverted into glutamate for use as a neurotransmitter or energy substrate.
“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: <scp><i>APOE3</i></scp> Christchurch homozygote glioprotection (2023) · cites this paper as [27]
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- Authors
- Son, H., Kim, S., Jung, D.-H., Baek, J. H., Lee, D. H., Roh, G. S., Kang, S. S., Cho, G. J., Choi, W. S., Lee, D. K., & Kim, H. J.
- Affiliations
- Gyeongsang National University (KR)
- Corresponding author
- Kim, Hyun Joon
- ORCID
- Venue
- Scientific Reports
- Published
- 2019-01-22
- Volume
- 9
- Issue
- 1
- Pages
- 252-252
- ISSN
- 2045-2322 (ISSN-L)
- PMC
- PMC6342969
- OpenAlex
- W2911887271
- Cited by
- 39
- References
- 47
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 5 · 2023: 6 · 2022: 9 · 2021: 7 · 2020: 4 · 2019: 1
- FWCI
- 2.51
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- Scientific Reports (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Research Foundation (2015R1A5A2008833)
- 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 › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Keywords
- glutamine synthetase, synaptogenesis, astrocytes, glutamatergic synapses, spatial memory impairment, hippocampal CA3, glial fibrillary acidic protein, postnatal development, glutamatergic neurotransmission
- MeSH terms
- Behavior Observation Techniques, Animals, Animals, Newborn, Astrocytes, Behavior, Animal, Glial Fibrillary Acidic Protein, Glutamine, Glutamate-Ammonia Ligase, Male, Methionine Sulfoximine, Synaptic Transmission, Neurons, Glutamic Acid, Models, Animal, Mice, Neurogenesis, CA3 Region, Hippocampal, Spatial Memory
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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