The DOI matches its Crossref record; 51 of the 51 references it cites were found in a registry or an index.
Cocaine triggered AMPA receptor redistribution is reversed in vivo by mGluR-dependent long-term depression
Open accessAbstract
Drugs of abuse induce long-lasting changes in neural circuits that may underlie core components of addiction. Here we focus on glutamatergic synapses onto dopamine (DA) neurons of the ventral tegmental area (VTA). Using an 'ex vivo' approach in mice, we show that a single injection of cocaine caused strong rectification and conferred sensitivity to the polyamine Joro spider toxin (JST) of AMPAR-mediated excitatory postsynaptic currents (AMPAR EPSCs), indicating the recruitment of receptors that lack GluR2. This qualitative change in transmission was paralleled by an increase in the AMPAR:NMDAR ratio and was prevented by interfering with the protein interacting with C kinase-1 (PICK1) in vivo. Activation of metabotropic glutamate receptors (mGluR1s) by intraperitoneal injection of a positive modulator depotentiated synapses and abolished rectification in slices of cocaine-treated mice, revealing a mechanism to reverse cocaine-induced synaptic plasticity in vivo.
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“Calcium-permeable, GluA2-lacking AMPARs appear (Bellone and Lu ¨scher 2006), while NMDAR function is decreased.”
From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Bellone and Lüscher 2006
In the citing paper
“Calcium-permeable, GluA2-lacking AMPARs appear (Bellone and Lu ¨scher 2006), while NMDAR function is decreased.”
From NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD). (2012) · cites this paper as Bellone and Lüscher 2006
Citations
Cites
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Is there a common molecular pathway for addiction?
Nestler, E. J. (2005) · Nature Neuroscience · doi:10.1038/nn1578 · Cited by 1,388
Drugs of Abuse and Stress Trigger a Common Synaptic Adaptation in Dopamine Neurons
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Single cocaine exposure in vivo induces long-term potentiation in dopamine neurons
Ungless, M. A., Whistler, J. L., Malenka, R. C., & Bonci, A. (2001) · Nature · doi:10.1038/35079077 · Cited by 1,106
Pierce, R. C., & Kumaresan, V. (2006) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2005.04.016 · Cited by 913
GRIP: a synaptic PDZ domain-containing protein that interacts with AMPA receptors
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Postsynaptic signaling and plasticity mechanisms
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Cited by
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Synaptic Plasticity: Multiple Forms, Functions, and Mechanisms
Citri, A., & Malenka, R. C. (2008) · Neuropsychopharmacology · doi:10.1038/sj.npp.1301559 · Cited by 2,323
Synaptic plasticity and addiction
Kauer, J. A., & Malenka, R. C. (2007) · Nature Reviews Neuroscience · doi:10.1038/nrn2234 · Cited by 1,397
NMDA receptor-dependent long-term potentiation and long-term depression (LTP/LTD).
Luscher, C., & Malenka, R. C. (2012) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a005710 · Cited by 1,110
Self-citationDrug-evoked synaptic plasticity in addiction: from molecular changes to circuit remodeling
Lüscher, C., & Malenka, R. C. (2011) · Neuron · doi:10.1016/j.neuron.2011.01.017 · Cited by 1,105
Self-citationSynaptic AMPA receptor plasticity and behavior
Kessels, H. W., & Malinow, R. (2009) · Neuron · doi:10.1016/j.neuron.2009.01.015 · Cited by 993
Metadata
- Authors
- Bellone, C., & Lüscher, C.
- Affiliations
- University of Geneva (CH)
- Corresponding author
- Lüscher, Christian
- Venue
- Nature Neuroscience
- Published
- 2006-04-02
- Volume
- 9
- Issue
- 5
- Pages
- 636-641
- ISSN
- 1097-6256 (ISSN-L)
- 1546-1726
- OpenAlex
- W2042529649
- Cited by
- 429
- References
- 51
- Citations by year
- 2026: 6 · 2025: 5 · 2024: 16 · 2023: 8 · 2022: 21 · 2021: 19 · 2020: 11 · 2019: 15 · 2018: 25 · 2017: 19 · 2016: 28 · 2015: 17 · 2014: 22 · 2013: 34 · 2012: 31
- FWCI
- 10.44
- Type
- journal article
- Language
- en
- Open access
- Licence
- Locations
- Nature Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Archive ouverte UNIGE (University of Geneva) (submittedVersion, cc-by)
- Funders
- Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Keywords
- cocaine, metabotropic glutamate receptor 1, long-term depression, depotentiation, ventral tegmental area, dopaminergic neurons, GluR2, PICK1, synaptic plasticity, addiction, glutamatergic synapses, joro spider toxin
- MeSH terms
- Animals, Animals, Newborn, Carrier Proteins, Cocaine, Dose-Response Relationship, Radiation, Drug Interactions, Electric Stimulation, Enzyme Inhibitors, Methoxyhydroxyphenylglycol, Mice, Inbred C57BL, Synaptic Transmission, Neurons, Nuclear Proteins, Ventral Tegmental Area, Receptors, AMPA, Receptors, Metabotropic Glutamate, Patch-Clamp Techniques, Dopamine Antagonists, Statistics, Nonparametric, Dopamine Uptake Inhibitors, Cell Cycle Proteins, Excitatory Postsynaptic Potentials, Long-Term Synaptic Depression, Mice, In Vitro Techniques
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