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Orexin A Phosphorylates the gamma-Aminobutyric Acid Type A Receptor beta(2) Subunit on a Serine Residue and Changes the Surface Expression of the Receptor in SH-SY5Y Cells Exposed to Propofol
Linköping University, Faculty of Medicine and Health Sciences. Östergötlands Läns Landsting, Anaesthetics, Operations and Specialty Surgery Center, Department of Anaesthesiology and Intensive Care in Linköping. Linköping University, Department of Medical and Health Sciences, Division of Drug Research.
Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Department of Anaesthesiology and Intensive Care in Linköping. Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences.
Linköping University, Department of Medical and Health Sciences, Division of Drug Research. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Anaesthetics, Operations and Specialty Surgery Center, Department of Anaesthesiology and Intensive Care in Linköping.
Linköping University, Department of Clinical and Experimental Medicine, Division of Clinical Sciences. Linköping University, Faculty of Medicine and Health Sciences.
2015 (English)In: Journal of Neuroscience Research, ISSN 0360-4012, E-ISSN 1097-4547, Vol. 93, no 11, 1748-1755 p.Article in journal (Refereed) Published
Abstract [en]

Propofol activates the gamma-aminobutyric acid type A receptor (GABA(A)R) and causes a reversible neurite retraction, leaving a thin, thread-like structure behind; it also reverses the transport of vesicles in rat cortical neurons. The awakening peptide orexin A (OA) inhibits this retraction via phospholipase D (PLD) and protein kinase CE (PKCE). The human SH-SY5Y cells express both GABA(A)Rs and orexin 1 and 2 receptors. These cells are used to examine the interaction between OA and the GABAAR. The effects of OA are studied with flow cytometry and immunoblotting. This study shows that OA stimulates phosphorylation on the serine residues of the GABA(A)R beta(2) subunit and that the phosphorylation is caused by the activation of PLD and PKCE. OA administration followed by propofol reduces the cell surface expression of the GABA(A)R, whereas propofol stimulation before OA increases the surface expression. The GABA(A)R beta(2) subunit is important for receptor recirculation, and the effect of OA on propofol-stimulated cells may be due to a disturbed recirculation of the GABA(A)R. (C) 2015 Wiley Periodicals, Inc.

Place, publisher, year, edition, pages
WILEY-BLACKWELL , 2015. Vol. 93, no 11, 1748-1755 p.
Keyword [en]
orexin; propofol; GABAAR; cell signaling; AB_10675844; AB_1269637; AB_10712311; AB_2247467; AB_307187; AB_307184; AB_1566589
National Category
Cell and Molecular Biology
Identifiers
URN: urn:nbn:se:liu:diva-122517DOI: 10.1002/jnr.23631ISI: 000362831800013PubMedID: 26283475OAI: oai:DiVA.org:liu-122517DiVA: diva2:868052
Note

Funding Agencies|County Council of Ostergotland ALF Grants; Linkoping University Hospital; Ella and Henry Stahl Research Foundation

Available from: 2015-11-09 Created: 2015-11-06 Last updated: 2016-04-12

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Andersson, HenrikBjörnström-Karlsson, KarinEintrei, ChristinaSundqvist, Tommy
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Faculty of Medicine and Health SciencesDepartment of Anaesthesiology and Intensive Care in LinköpingDivision of Drug ResearchDepartment of Anaesthesiology and Intensive Care in LinköpingDivision of Clinical Sciences
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Journal of Neuroscience Research
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