Cannabinoid agonists increase the interaction between β-Arrestin 2 and ERK1/2 and upregulate β-Arrestin 2 and 5-HT(2A) receptors

We have recently reported that selective cannabinoid 2 (CB(2)) receptor agonists upregulate 5-HT(2A) receptors by enhancing ERK1/2 signaling in prefrontal cortex (PFCx). Increased activity of cortical 5-HT(2A) receptors has been associated with several neuropsychiatric disorders such as anxiety and...

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Veröffentlicht in:	Pharmacological research 2013-02, Vol.68 (1), p.46
Hauptverfasser:	Franklin, Jade M, Vasiljevik, Tamara, Prisinzano, Thomas E, Carrasco, Gonzalo A
Format:	Artikel
Sprache:	eng
Schlagworte:	Animals Arrestins - biosynthesis Arrestins - genetics beta-Arrestin 2 beta-Arrestins Cannabinoid Receptor Agonists - pharmacology Cannabinoid Receptor Antagonists - pharmacology Concanavalin A - pharmacology Cyclohexanols - pharmacology Male Mitogen-Activated Protein Kinase 1 - antagonists & inhibitors Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - antagonists & inhibitors Mitogen-Activated Protein Kinase 3 - metabolism Protein Kinase Inhibitors - pharmacology Rats Rats, Sprague-Dawley Receptor, Cannabinoid, CB1 - agonists Receptor, Cannabinoid, CB1 - antagonists & inhibitors Receptor, Cannabinoid, CB1 - genetics Receptor, Cannabinoid, CB2 - agonists Receptor, Cannabinoid, CB2 - antagonists & inhibitors Receptor, Cannabinoid, CB2 - genetics Receptor, Serotonin, 5-HT2A - biosynthesis RNA, Messenger - metabolism RNA, Small Interfering - genetics Up-Regulation
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