ArticlePloS one2012
Nicotine uses neuron-glia communication to enhance hippocampal synaptic transmission and long-term memory.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 31 citations in OpenAlex.
- D-serine: A Multitalented Neuromodulator in Brain Function, Systemic Homeostasis, and Disease.Cellular and molecular neurobiology · 2026Review
- Nicotine is an Immunosuppressant: Implications for Women's Health and Disease.Journal of neuroimmunology · 2024Review
- Nicotine induces morphological and functional changes in astrocytes via nicotinic receptor activity.Glia · 2021Article
- Glial cells as therapeutic targets for smoking cessation.Neuropharmacology · 2020Review
- Review
- Astrocytes as Guardians of Neuronal Excitability: Mechanisms Underlying Epileptogenesis.Frontiers in neurology · 2020Review
- Molecular Insights Into Memory-Enhancing Metabolites of Nicotine in Brain: A Systematic Review.Frontiers in neuroscience · 2018Article
- Formation of Opioid-Induced Memory and Its Prevention: A Computational Study.Frontiers in computational neuroscience · 2018Article
- Gene expression profiling of midbrain dopamine neurons upon gestational nicotine exposure.Medical & biological engineering & computing · 2017Article
- Astrocyte Calcium Responses to Sensory Input: Influence of Circuit Organization and Experimental Factors.Frontiers in neural circuits · 2017Review
- Enteric Glial Cells: A New Frontier in Neurogastroenterology and Clinical Target for Inflammatory Bowel Diseases.Inflammatory bowel diseases · 2016Review
- Volume transmission signalling via astrocytes.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2014Review
- Cell-type specific mechanisms of D-serine uptake and release in the brain.Frontiers in synaptic neuroscience · 2014Review
- The role of astrocytes in the regulation of synaptic plasticity and memory formation.Neural plasticity · 2013Review
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nicotine enhances synaptic transmission and facilitates long-term memory. Now it is known that bi-directional glia-neuron interactions play important roles in the physiology of the brain. However, the involvement of glial cells in the effects of nicotine has not been considered until now. In particular, the gliotransmitter D-serine, an endogenous co-agonist of NMDA receptors, enables different types of synaptic plasticity and memory in the hippocampus. Here, we report that hippocampal long-term synaptic plasticity induced by nicotine was annulled by an enzyme that degrades endogenous D-serine, or by an NMDA receptor antagonist that acts at the D-serine binding site. Accordingly, both effects of nicotine: the enhancement of synaptic transmission and facilitation of long-term memory were eliminated by impairing glial cells with fluoroacetate, and were restored with exogenous D-serine. Together, these results show that glial D-serine is essential for the long-term effects of nicotine on synaptic plasticity and memory, and they highlight the roles of glial cells as key participants in brain functions.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.