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Differential expression of delta opioid receptors and mRNA in proliferating astrocytes during the cell cycle

2000; Wiley; Volume: 61; Issue: 4 Linguagem: Inglês

10.1002/1097-4547(20000815)61

1097-4547

Anders I. Persson, Thorleif Thorlin, Lars R�nnb�ck, Elisabeth Hansson, Peter S. Eriksson,

Pharmacological Receptor Mechanisms and Effects

Journal of Neuroscience ResearchVolume 61, Issue 4 p. 371-375 Article Differential expression of delta opioid receptors and mRNA in proliferating astrocytes during the cell cycle P. Anders I. Persson, P. Anders I. Persson Institute of Clinical Neuroscience, Göteborg University, Göteborg, SwedenSearch for more papers by this authorThorleif Thorlin, Thorleif Thorlin Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden Institute of Neurobiology, Göteborg University, Göteborg, SwedenSearch for more papers by this authorLars Rönnbäck, Lars Rönnbäck Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden Institute of Neurobiology, Göteborg University, Göteborg, SwedenSearch for more papers by this authorElisabeth Hansson, Elisabeth Hansson Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden Institute of Neurobiology, Göteborg University, Göteborg, SwedenSearch for more papers by this authorPeter S. Eriksson, Corresponding Author Peter S. Eriksson [email protected] Institute of Clinical Neuroscience, Göteborg University, Göteborg, SwedenInstitute of Clinical Neuroscience, Göteborg University, Blå Stråket 7, Sahlgren's University Hospital, SE-413 45 Göteborg, SwedenSearch for more papers by this author P. Anders I. Persson, P. Anders I. Persson Institute of Clinical Neuroscience, Göteborg University, Göteborg, SwedenSearch for more papers by this authorThorleif Thorlin, Thorleif Thorlin Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden Institute of Neurobiology, Göteborg University, Göteborg, SwedenSearch for more papers by this authorLars Rönnbäck, Lars Rönnbäck Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden Institute of Neurobiology, Göteborg University, Göteborg, SwedenSearch for more papers by this authorElisabeth Hansson, Elisabeth Hansson Institute of Clinical Neuroscience, Göteborg University, Göteborg, Sweden Institute of Neurobiology, Göteborg University, Göteborg, SwedenSearch for more papers by this authorPeter S. Eriksson, Corresponding Author Peter S. Eriksson [email protected] Institute of Clinical Neuroscience, Göteborg University, Göteborg, SwedenInstitute of Clinical Neuroscience, Göteborg University, Blå Stråket 7, Sahlgren's University Hospital, SE-413 45 Göteborg, SwedenSearch for more papers by this author First published: 31 July 2000 https://doi.org/10.1002/1097-4547(20000815)61:4 3.0.CO;2-HCitations: 18AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat Abstract Previous immunohistochemical and radioligand binding studies have shown a cell cycle-dependent regulation of the delta opioid receptor (DOR). The relationship between DOR expression and mitosis in primary astroglial cultures of rat cerebral cortex was investigated in this study. The cultures were arrested during the G1/S transition or during mitosis. The DOR protein level increased twofold (P = 0.009) during mitosis and DOR mRNA level increased threefold (P = 0.002) during the G1/S transition compared to nonsynchronized cultures. DOR mRNA was also elevated (1.6-fold, P = 0.008) during the G1/S transition compared with mitotic cells. A premitotic increase in DOR mRNA suggests that elevated DOR protein levels during mitosis might be regulated during transcription. J. Neurosci. Res. 61:371–375, 2000. © 2000 Wiley-Liss, Inc. 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