Cross-Talk between Protein Kinase A and Mitogen-Activated Protein Kinases Signalling in the Adaptive Changes Observed during Morphine Withdrawal in the Heart
The Journal of Pharmacology and Experimental Therapeutics, ISSN: 0022-3565, Vol: 330, Issue: 3, Page: 771-782
2009
- 4Citations
- 14Captures
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Metrics Details
- Citations4
- Citation Indexes4
- CrossRef2
- Captures14
- Readers14
- 14
Article Description
Our previous studies have shown that morphine withdrawal induced an increase in the expression of protein kinase (PK) A and mitogen-activated extracellular kinase (MAPK) pathways in the heart during morphine withdrawal. The purpose of the present study was to evaluate the interaction between PKA and extracellular signal-regulated kinase (ERK) signaling pathways mediating the cardiac adaptive changes observed after naloxone administration to morphine-dependent rats. Dependence on morphine was induced by a 7-day subcutaneous implantation of morphine pellets. Morphine withdrawal was precipitated on day 8 by an injection of naloxone (2 mg/kg). ERK1/2 and tyrosine hydroxylase (TH) phosphorylation was determined by quantitative blot immunolabeling using phosphorylation state-specific antibodies. Naloxone-induced morphine withdrawal activates ERK1/2 and phosphorylates TH at Ser31 in the right and left ventricle, with an increase in the mean arterial blood pressure and heart rate. When N -(2-guanidinoethyl)-5-isoquinolinesulfonamide (HA-1004), a PKA inhibitor, was infused, concomitantly with morphine, it diminished the expression of ERK1/2. In contrast, the infusion of calphostin C (a PKC inhibitor) did not modify the morphine withdrawal-induced activation of ERK1/2. The ability of morphine withdrawal to activate ERK that phosphorylates TH at Ser31 was reduced by HA-1004. The present findings demonstrate that the enhancement of ERK1/2 expression and the phosphorylation state of TH at Ser31 during morphine withdrawal are dependent on PKA and suggest cross-talk between PKA and ERK1/2 transduction pathway mediating morphine withdrawal-induced activation (phosphorylation) of TH.
Bibliographic Details
http://www.sciencedirect.com/science/article/pii/S0022356524385751; http://dx.doi.org/10.1124/jpet.109.154583; http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=70349141426&origin=inward; http://www.ncbi.nlm.nih.gov/pubmed/19567779; https://linkinghub.elsevier.com/retrieve/pii/S0022356524385751; https://dx.doi.org/10.1124/jpet.109.154583; https://jpet.aspetjournals.org/content/330/3/771
Elsevier BV
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