ArticleBritish journal of pharmacology1999
Parallel modulation of receptor for activated C kinase 1 and protein kinase C-alpha and beta isoforms in brains of morphine-treated rats.
Article in British journal of pharmacology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 27 citations in OpenAlex.
- S-Glutathionylation and Redox Protein Signaling in Drug Addiction.Progress in molecular biology and translational science · 2016Article
- RACK1, A multifaceted scaffolding protein: Structure and function.Cell communication and signaling : CCS · 2011Article
- Chronic morphine treatment impaired hippocampal long-term potentiation and spatial memory via accumulation of extracellular adenosine acting on adenosine A1 receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Phosphorylation of GluR1, ERK, and CREB during spontaneous withdrawal from chronic heroin self-administration.Synapse (New York, N.Y.) · 2009Article
- Effect of long-term exposure of SH-SY5Y cells to morphine: a whole cell proteomic analysis.Proteome science · 2006Article
- Protein kinase C isozymes and addiction.Molecular neurobiology · 2004Review
- Morphine withdrawal increases glutamate uptake and surface expression of glutamate transporter GLT1 at hippocampal synapses.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2003Article
- Parallel modulation of receptor for activated C kinase 1 and protein kinase C-alpha and beta isoforms in brains of morphine-treated rats.British journal of pharmacology · 1999Article
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2 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
1. Receptor for activated C kinase 1 (RACK1) is an intracellular receptor for protein kinase C (PKC) that regulates the cellular enzyme localization. Because opiate drugs modulate the levels of brain PKC (Ventayol et al., 1997), the aim of this study was to assess in parallel the effects of morphine on RACK1 and PKC-alpha and beta isozymes densities in rat brain frontal cortex by immunoblot assays. 2. Acute morphine (30 mg kg(-1), i.p., 2 h) induced significant increases in the densities of RACK1 (33%), PKC-alpha (35%) and PKC-beta (23%). In contrast, chronic morphine (10-100 mg kg(-1), i.p., 5 days) induced a decrease in RACK1 levels (22%), paralleled by decreases in the levels of PKC-alpha (16%) and PKC-beta (16%). 3. Spontaneous (48 h) and naloxone (2 mg kg(-1), i.p., 2 h)-precipitated morphine withdrawal after chronic morphine induced marked up-regulations in the levels of RACK1 (38-41%), PKC-alpha (51-52%) and PKC-beta (48-62%). 4. In the same brains and for all combined treatments, there were significant positive correlations between the density of RACK1 and those of PKC-alpha (r=0.85, n = 35) and PKC-beta (r=0.75, n=32). 5. These data indicate that RACK1 is involved in the short- and long-term effects of morphine and in opiate withdrawal, and that RACK1 modulation by morphine or its withdrawal is parallel to those of PKC-alpha and beta isozymes. Since RACK1 facilitates the PKC substrate accessibility, driving its cellular localization, the coordinate regulation of the PKC/RACK system by morphine could be a relevant molecular mechanism in opiate addiction.
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