ArticleLife sciences2013
PKA and ERK1/2 are involved in dopamine D₁ receptor-induced heterologous desensitization of the δ opioid receptor.
Article in Life sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 11 citations in OpenAlex.
- Dopamine-Induced Ascorbate Release From Retinal Neurons Involves Glutamate Release, Activation of AMPA/Kainate Receptors and Downstream Signaling Pathways.Frontiers in neuroscience · 2019Article
- Identification of a signaling cascade that maintains constitutive δ-opioid receptor incompetence in peripheral sensory neurons.The Journal of biological chemistry · 2017Article
- Functional Characterization of a Novel Series of Biased Signaling Dopamine D3 Receptor Agonists.ACS chemical neuroscience · 2017Article
- Molecular Pharmacology of δ-Opioid Receptors.Pharmacological reviews · 2016Review
- The orexin 1 receptor modulates kappa opioid receptor function via a JNK-dependent mechanism.Cellular signalling · 2015Article
- Opioid receptor desensitization: mechanisms and its link to tolerance.Frontiers in pharmacology · 2014Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
aimsChronic administration of cocaine attenuates delta opioid receptor (DOPR) signaling in the striatum and the desensitization is mediated by the indirect actions of cocaine on dopamine D1 receptors (D1R). In addition, DOPR and D1R co-exist in some rat striatal neurons. In the present study, we examined the underlying mechanism of DOPR desensitization by D1R activation. MAIN
methodsNG 108-15 cells stably expressing HA-rat D1 receptor (HA-D1R) and Chinese hamster ovary (CHO) cells stably expressing both FLAG-mouse DOPR (FLAG-DOPR) and HA-D1R were used as the cell models. Receptor binding, [(35)S]GTPγS binding, receptor phosphorylation and western blot were conducted to examine DOPR affinity, expression, internalization, downregulation, desensitization, phosphorylation and phosphorylated ERK1/2. KEY
findingsPretreatment with either the DOPR agonist DPDPE or the D1R agonist SKF-82958 for 30min attenuated DPDPE-stimulated [(35)S]GTPγS binding to G proteins, demonstrating homologous and heterologous desensitization of the DOPR, respectively. SKF-82958 pretreatment did not affect the level of DOPR or affinity of DOPR antagonist or agonists, nor did it induce phosphorylation, internalization or down-regulation of the DOPR in the CHO-FLAG-DOPR/HA-D1R cells. Pretreatment of cells with inhibitors of PKA, MEK1 and PI3K, but not PKC, attenuated SKF-82958-induced desensitization of the DOPR. The D1R agonist SKF-82958 enhanced phosphorylation of ERK1/2, and pretreatment with inhibitors of MEK1 and PI3K, but not PKA and PKC, reduced the effect. These results indicate that activation of ERK1/2 and/or PKA, but not PKC, is involved in D1 receptor-induced heterologous desensitization of the DOPR. SIGNIFICANCE: This study provides possible mechanisms underlying D1R activation-induced DOPR desensitization.
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