دورية أكاديمية
Endocannabinoid regulation of nausea is mediated by 2-arachidonoylglycerol (2-AG) in the rat visceral insular cortex.
| العنوان: | Endocannabinoid regulation of nausea is mediated by 2-arachidonoylglycerol (2-AG) in the rat visceral insular cortex. |
|---|---|
| المؤلفون: | Sticht MA; Dept. of Psychology and Collaborative Neuroscience Program, University of Guelph, Guelph, Ontario, Canada; Hotchkiss Brain Institute, Dept. of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada. Electronic address: martin.sticht@ucalgary.ca., Limebeer CL; Dept. of Psychology and Collaborative Neuroscience Program, University of Guelph, Guelph, Ontario, Canada., Rafla BR; Dept. of Psychology and Collaborative Neuroscience Program, University of Guelph, Guelph, Ontario, Canada., Abdullah RA; Dept. of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA., Poklis JL; Dept. of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA., Ho W; Hotchkiss Brain Institute, Dept. of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada., Niphakis MJ; The Skaggs Institute for Chemical Biology and Dept. of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA., Cravatt BF; The Skaggs Institute for Chemical Biology and Dept. of Chemical Physiology, The Scripps Research Institute, La Jolla, CA, USA., Sharkey KA; Hotchkiss Brain Institute, Dept. of Physiology and Pharmacology, University of Calgary, Calgary, Alberta, Canada., Lichtman AH; Dept. of Pharmacology and Toxicology, Medical College of Virginia Campus, Virginia Commonwealth University, Richmond, VA, USA., Parker LA; Dept. of Psychology and Collaborative Neuroscience Program, University of Guelph, Guelph, Ontario, Canada. |
| المصدر: | Neuropharmacology [Neuropharmacology] 2016 Mar; Vol. 102, pp. 92-102. Date of Electronic Publication: 2015 Nov 02. |
| نوع المنشور: | Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
| اللغة: | English |
| بيانات الدورية: | Publisher: Pergamon Press Country of Publication: England NLM ID: 0236217 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1873-7064 (Electronic) Linking ISSN: 00283908 NLM ISO Abbreviation: Neuropharmacology Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Oxford : Pergamon Press Original Publication: Oxford, New York, Pergamon. |
| مواضيع طبية MeSH: | Arachidonic Acids/*metabolism , Cerebral Cortex/*metabolism , Endocannabinoids/*metabolism , Glycerides/*metabolism , Nausea/*metabolism, Animals ; Carbamates/pharmacology ; Cerebral Cortex/drug effects ; Neurons/drug effects ; Neurons/metabolism ; Piperazines/pharmacology ; Proto-Oncogene Proteins c-fos/metabolism ; Rats ; Receptor, Cannabinoid, CB1/metabolism |
| مستخلص: | Cannabinoid (CB) agonists suppress nausea in humans and animal models; yet, their underlying neural substrates remain largely unknown. Evidence suggests that the visceral insular cortex (VIC) plays a critical role in nausea. Given the expression of CB1 receptors and the presence of endocannabinoids in this brain region, we hypothesized that the VIC endocannabinoid system regulates nausea. In the present study, we assessed whether inhibiting the primary endocannabinoid hydrolytic enzymes in the VIC reduces acute lithium chloride (LiCl)-induced conditioned gaping, a rat model of nausea. We also quantified endocannabinoid levels during an episode of nausea, and assessed VIC neuronal activation using the marker, c-Fos. Local inhibition of monoacylglycerol lipase (MAGL), the main hydrolytic enzyme of 2-arachidonylglycerol (2-AG), reduced acute nausea through a CB1 receptor mechanism, whereas inhibition of fatty acid amide hydrolase (FAAH), the primary catabolic enzyme of anandamide (AEA), was without effect. Levels of 2-AG were also selectively elevated in the VIC during an episode of nausea. Inhibition of MAGL robustly increased 2-AG in the VIC, while FAAH inhibition had no effect on AEA. Finally, we demonstrated that inhibition of MAGL reduced VIC Fos immunoreactivity in response to LiCl treatment. Taken together, these findings provide compelling evidence that acute nausea selectively increases 2-AG in the VIC, and suggests that 2-AG signaling within the VIC regulates nausea by reducing neuronal activity in this forebrain region. (Copyright © 2015 Elsevier Ltd. All rights reserved.) |
| References: | Psychopharmacology (Berl). 2003 Mar;166(2):156-62. (PMID: 12528012) Biochem Pharmacol. 1995 Jun 29;50(1):83-90. (PMID: 7605349) Learn Behav. 2003 May;31(2):165-72. (PMID: 12882375) Brain Res. 1978 Mar 24;143(2):263-79. (PMID: 630409) Science. 1978 Jul 21;201(4352):267-9. (PMID: 663655) Gen Pharmacol. 1986;17(3):333-7. (PMID: 2424806) Brain Res. 1986 Aug 6;379(2):329-41. (PMID: 3742225) J Comp Neurol. 1987 Aug 1;262(1):27-45. (PMID: 2442207) Integr Physiol Behav Sci. 2003 Apr-Jun;38(2):133-45. (PMID: 14527182) J Comp Neurol. 1991 Sep 1;311(1):1-16. (PMID: 1719041) Brain Res. 1991 Aug 9;556(1):95-100. (PMID: 1718560) Eur J Pharmacol. 2004 Mar 19;488(1-3):201-12. (PMID: 15044052) Behav Neurosci. 1992 Feb;106(1):140-6. (PMID: 1313241) Science. 1992 Dec 18;258(5090):1946-9. (PMID: 1470919) Biochem Biophys Res Commun. 1995 Oct 4;215(1):89-97. (PMID: 7575630) Nature. 1996 Nov 7;384(6604):83-7. (PMID: 8900284) J Pharmacol Exp Ther. 2005 Apr;313(1):352-8. (PMID: 15579492) Science. 2005 Oct 14;310(5746):329-32. (PMID: 16224028) Auton Neurosci. 2006 Apr 30;125(1-2):100-15. (PMID: 16556512) Behav Brain Res. 2006 Jun 30;170(2):271-6. (PMID: 16603254) Neuroscience. 2007 May 25;146(3):1212-9. (PMID: 17383106) Science. 2007 Oct 26;318(5850):655-8. (PMID: 17962567) Appetite. 2008 Mar-May;50(2-3):430-4. (PMID: 17996982) Cereb Cortex. 2008 Jun;18(6):1292-301. (PMID: 17921459) Bioorg Med Chem Lett. 2008 Nov 15;18(22):5875-8. (PMID: 18752948) Chem Biol. 2009 Apr 24;16(4):411-20. (PMID: 19389627) Int Rev Neurobiol. 2009;85:57-72. (PMID: 19607961) Proc Natl Acad Sci U S A. 2009 Dec 1;106(48):20270-5. (PMID: 19918051) Aviat Space Environ Med. 2011 Apr;82(4):424-33. (PMID: 21485400) Neuropharmacology. 2011 Dec;61(7):1070-87. (PMID: 21669214) J Pharmacol Exp Ther. 2011 Oct;339(1):173-85. (PMID: 21719468) Science. 2011 Nov 11;334(6057):809-13. (PMID: 22021672) Physiol Behav. 2012 Feb 1;105(3):856-60. (PMID: 22056540) Br J Pharmacol. 2012 Apr;165(8):2425-35. (PMID: 21470205) Eur Neuropsychopharmacol. 2012 Sep;22(9):664-71. (PMID: 22325231) J Neurosci. 2012 Oct 3;32(40):13709-17. (PMID: 23035083) Br J Pharmacol. 2012 Nov;167(5):1126-36. (PMID: 22671779) Neuropharmacology. 2013 Feb;65:83-9. (PMID: 23000076) Life Sci. 2013 Mar 19;92(8-9):458-62. (PMID: 22705310) Cereb Cortex. 2013 Apr;23(4):806-13. (PMID: 22473843) J Pharmacol Exp Ther. 2013 Jun;345(3):492-501. (PMID: 23412396) Eur J Pharmacol. 2014 Jan 5;722:134-46. (PMID: 24184696) Expert Opin Investig Drugs. 2014 Aug;23(8):1123-40. (PMID: 24836296) Neuroscience. 2015 Feb 12;286:338-44. (PMID: 25499318) Psychopharmacology (Berl). 2015 Feb;232(3):583-93. (PMID: 25085768) Clin Pharmacol Ther. 2015 Jun;97(6):559-61. (PMID: 25691302) Psychopharmacology (Berl). 2015 Oct;232(20):3841-8. (PMID: 26297326) Cereb Cortex. 2016 Feb;26(2):485-97. (PMID: 25115821) Proc Natl Acad Sci U S A. 2014 Dec 23;111(51):18333-8. (PMID: 25489086) Neuroreport. 1999 Dec 16;10(18):3769-72. (PMID: 10716207) Am J Med. 2001 Dec 3;111 Suppl 8A:106S-112S. (PMID: 11749934) Science. 1974 Sep 6;185(4154):824-31. (PMID: 11785521) Neuroscience. 2002;109(3):451-60. (PMID: 11823058) Proc Natl Acad Sci U S A. 2002 Aug 6;99(16):10819-24. (PMID: 12136125) Br J Pharmacol. 2002 Nov;137(5):589-96. (PMID: 12381672) Psychopharmacology (Berl). 2003 Mar;166(2):120-6. (PMID: 12552358) |
| معلومات مُعتمدة: | R01DA032933 United States DA NIDA NIH HHS; P30 DA033934 United States DA NIDA NIH HHS; R01 DA032933 United States DA NIDA NIH HHS; 334086 Canada Canadian Institutes of Health Research; P01 DA009789 United States DA NIDA NIH HHS; P30DA033934 United States DA NIDA NIH HHS; P01DA009789 United States DA NIDA NIH HHS |
| فهرسة مساهمة: | Keywords: 2-arachidonoylglycerol (2-AG); 25154867); Anandamide (PubChem CID: 5281969); Endocannabinoid; Insular cortex; JZL195 (PubChem CID: 46232606); Lithium chloride (PubChem CID: 433294); MJN110 (PubChem CID: N/A); Monoacylglycerol lipase (MAGL); Nausea; Oleoylethanolamide (PubChem CID: 5283454); PF3845 (PubChem CID:; Palmitoylethanolamide (PubChem CID: 4671); Saccharin (PubChem CID: 5143); Tween 80 (PubChem CID: 5281955); URB597 (PubChem CID: 1383884); c-Fos |
| المشرفين على المادة: | 0 (Arachidonic Acids) 0 (Carbamates) 0 (Endocannabinoids) 0 (Glycerides) 0 (JZL195) 0 (Piperazines) 0 (Proto-Oncogene Proteins c-fos) 0 (Receptor, Cannabinoid, CB1) 8D239QDW64 (glyceryl 2-arachidonate) |
| تواريخ الأحداث: | Date Created: 20151107 Date Completed: 20161007 Latest Revision: 20181113 |
| رمز التحديث: | 20231215 |
| مُعرف محوري في PubMed: | PMC4698202 |
| DOI: | 10.1016/j.neuropharm.2015.10.039 |
| PMID: | 26541329 |
| قاعدة البيانات: | MEDLINE |
Full Text Finder كن أول من يترك تعليقا!