ArticleiScience2019
Inhibiting Glutamate Activity during Consolidation Suppresses Age-Related Long-Term Memory Impairment in Drosophila.
Article in iScience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 28 citations in OpenAlex.
- Aberrant dopaminergic activity during consolidation causes age-related memory generalization in Drosophila.PLoS biology · 2026Article
- Molecular profiling of invertebrate glia.Glia · 2025Review
- Biological aging of two innate behaviors of Drosophila melanogaster: Escape climbing versus courtship learning and memory.PloS one · 2024Article
- Can RNA Affect Memory Modulation? Implications for PTSD Understanding and Treatment.International journal of molecular sciences · 2023Review
- Article
- Sleep benefits different stages of memory inFrontiers in physiology · 2023Review
- Novel EAAT2 activators improve motor and cognitive impairment in a transgenic model of Huntington's disease.Frontiers in behavioral neuroscience · 2023Article
- Age-related memory vulnerability to interfering stimuli is caused by gradual loss of MAPK-dependent protection in Drosophila.Aging cell · 2022Article
- TheGenome research · 2021Article
- Sesamin Activates Nrf2/Cnc-Dependent Transcription in the Absence of Oxidative Stress inAntioxidants (Basel, Switzerland) · 2021Article
- Post-Developmental Roles of Notch Signaling in the Nervous System.Biomolecules · 2020Review
- Spatially-resolved metabolic profiling of living Drosophila in neurodegenerative conditions usingScientific reports · 2020Article
- Octopamine neuron dependent aggression requires dVGLUT from dual-transmitting neurons.PLoS genetics · 2020Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In Drosophila, long-term memory (LTM) formation requires increases in glial gene expression. Klingon (Klg), a cell adhesion molecule expressed in both neurons and glia, induces expression of the glial transcription factor, Repo. However, glial signaling downstream of Repo has been unclear. Here we demonstrate that Repo increases expression of the glutamate transporter, EAAT1, and EAAT1 is required during consolidation of LTM. The expressions of Klg, Repo, and EAAT1 decrease upon aging, suggesting that age-related impairments in LTM are caused by dysfunction of the Klg-Repo-EAAT1 pathway. Supporting this idea, overexpression of Repo or EAAT1 rescues age-associated impairments in LTM. Pharmacological inhibition of glutamate activity during consolidation improves LTM in klg mutants and aged flies. Altogether, our results indicate that LTM formation requires glial-dependent inhibition of glutamate signaling during memory consolidation, and aging disrupts this process by inhibiting the Klg-Repo-EAAT1 pathway.
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