ArticleNeuroscience letters2013
Acute cocaine increases phosphorylation of CaMKII and GluA1 in the dorsolateral striatum of drug naïve rats, but not cocaine-experienced rats.
Article in Neuroscience letters, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- D1 receptor hypersensitivity in mice with low striatal D2 receptors facilitates select cocaine behaviors.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2019Article
- A Critical Role for the GluA1 Accessory Protein, SAP97, in Cocaine Seeking.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2016Article
- Oxytocin reduces cocaine seeking and reverses chronic cocaine-induced changes in glutamate receptor function.The international journal of neuropsychopharmacology · 2014Article
- αCaMKII controls the establishment of cocaine's reinforcing effects in mice and humans.Translational psychiatry · 2014Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Transport of GluA1-containing AMPA glutamate receptors to synapses in the nucleus accumbens, a process that involves phosphorylation of key serine residues by CaMKII, is associated with the reinstatement of cocaine-seeking behavior. A growing body of evidence indicates that the dorsal striatum contributes to aspects of cocaine addiction. However, the potential role of CaMKII-mediated phosphorylation of GluA1 subunits in the dorsolateral (DL) striatum during cocaine reinstatement has not been examined. In this study, rats were trained to self-administer cocaine and were partnered with saline-yoked rats that received injections of saline. Following extinction, each pair of rats received either a systemic priming injection of cocaine (10mg/kg, i.p.) or saline. As expected, cocaine-experienced rats displayed robust reinstatement of cocaine seeking in response to a challenge injection, whereas yoked saline controls did not. The DL striatum was dissected immediately following the reinstatement test session. Results from Western blotting experiments showed increased pGluA1-ser831 and pCaMKII-thr286 in the DL striatum of saline-yoked rats given an acute injection of cocaine. This effect was absent in cocaine-experienced rats that received a saline injection, and no changes were observed following a priming injection of cocaine in cocaine-experienced rats. These results indicate that acute exposure to cocaine in drug naïve rats increased CaMKII-mediated phosphorylation of GluA1-containing AMPA receptors in the DL striatum, an effect that was not observed during cocaine priming-induced reinstatement of drug seeking. It is possible; therefore, that increased phosphorylation of CaMKII and GluA1 following acute cocaine is a compensatory mechanism in the DL striatum.
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