ArticleFrontiers in cellular neuroscience2014
Nicotinic α7 receptor activation selectively potentiates the function of NMDA receptors in glutamatergic terminals of the nucleus accumbens.
Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 39 citations in OpenAlex.
- Trial
- Non-targeted and Targeted Metabolomics Techniques Reveal Striatal Metabolome Characteristics in the Ketamine-Induced Conditioned Place Preference Mice Model.Journal of molecular neuroscience : MN · 2025Article
- Article
- Synaptosomes and Metamodulation of Receptors.Methods in molecular biology (Clifton, N.J.) · 2022Article
- LiCl attenuates impaired learning and memory of APP/PS1 mice, which in mechanism involves α7 nAChRs and Wnt/β-catenin pathway.Journal of cellular and molecular medicine · 2021Article
- Presynaptic release-regulating NMDA receptors in isolated nerve terminals: A narrative review.British journal of pharmacology · 2021Review
- Does kynurenic acid act on nicotinic receptors? An assessment of the evidence.Journal of neurochemistry · 2020Review
- Immuno-Pharmacological Characterization of Presynaptic GluN3A-Containing NMDA Autoreceptors: Relevance to Anti-NMDA Receptor Autoimmune Diseases.Molecular neurobiology · 2019Article
- Effects of α7 Nicotinic Receptor Activation on Cell Survival in Rat Organotypic Hippocampal Slice Cultures.Neurotoxicity research · 2018Article
- Septal Cholinergic Neuromodulation Tunes the Astrocyte-Dependent Gating of Hippocampal NMDA Receptors to Wakefulness.Neuron · 2017Article
- Do specific NMDA receptor subunits act as gateways for addictive behaviors?Genes, brain, and behavior · 2017Review
- CCL5-Glutamate Cross-Talk in Astrocyte-Neuron Communication in Multiple Sclerosis.Frontiers in immunology · 2017Review
- Alpha7 Nicotinic Acetylcholine Receptors Play a Predominant Role in the Cholinergic Potentiation of N-Methyl-D-Aspartate Evoked Firing Responses of Hippocampal CA1 Pyramidal Cells.Frontiers in cellular neuroscience · 2017Article
- Modulation of excitatory neurotransmission by neuronal/glial signalling molecules: interplay between purinergic and glutamatergic systems.Purinergic signalling · 2016Review
- Nicotinic modulation of glutamate receptor function at nerve terminal level: a fine-tuning of synaptic signals.Frontiers in pharmacology · 2015Review
- Article
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Authors and funding
9 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We here provide functional and immunocytochemical evidence supporting the co-localization and functional interaction between nicotinic acetylcholine receptors (nAChRs) and N-methyl-D-aspartic acid receptors (NMDARs) in glutamatergic terminals of the nucleus accumbens (NAc). Immunocytochemical studies showed that a significant percentage of NAc terminals were glutamatergic and possessed GluN1 and α7-containing nAChR. A short-term pre-exposure of synaptosomes to nicotine (30 µM) or choline (1 mM) caused a significant potentiation of the 100 µM NMDA-evoked [(3)H]D-aspartate ([(3)H]D-Asp) outflow, which was prevented by α-bungarotoxin (100 nM). The pre-exposure to nicotine (100 µM) or choline (1 mM) also enhanced the NMDA-induced cytosolic free calcium levels, as measured by FURA-2 fluorescence imaging in individual NAc terminals, an effect also prevented by α-bungarotoxin. Pre-exposure to the α4-nAChR agonists 5IA85380 (10 nM) or RJR2429 (1 µM) did not modify NMDA-evoked ([(3)H]D-Asp) outflow and calcium transients. The NMDA-evoked ([(3)H]D-Asp) overflow was partially antagonized by the NMDAR antagonists MK801, D-AP5, 5,7-DCKA and R(-)CPP and unaffected by the GluN2B-NMDAR antagonists Ro256981 and ifenprodil. Notably, pre-treatment with choline increased GluN2A biotin-tagged proteins. In conclusion, our results show that the GluN2A-NMDA receptor function can be positively regulated in NAc terminals in response to a brief incubation with α7 but not α4 nAChRs agonists. This might be a general feature in different brain areas since a similar nAChR-mediated bolstering of NMDA-induced ([(3)H]D-Asp) overflow was also observed in hippocampal synaptosomes.
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