دورية أكاديمية
أعرض في EDS

Deletion of lynx1 reduces the function of α6* nicotinic receptors.

التفاصيل البيبلوغرافية
العنوان: Deletion of lynx1 reduces the function of α6* nicotinic receptors.
المؤلفون: Parker RL; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, United States of America., O'Neill HC; Institute for Behavioral Genetics, University of Colorado Boulder, Boulder, CO, United States of America., Henley BM; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, United States of America., Wageman CR; Institute for Behavioral Genetics, University of Colorado Boulder, Boulder, CO, United States of America., Drenan RM; Department of Pharmacology, Northwestern University Feinberg School of Medicine, Chicago, IL, United States of America., Marks MJ; Institute for Behavioral Genetics, University of Colorado Boulder, Boulder, CO, United States of America.; Department of Psychology and Neuroscience, University of Colorado, Boulder, CO, United States of America., Miwa JM; Department of Biological Sciences, Lehigh University, Bethlehem, PA, United States of America., Grady SR; Institute for Behavioral Genetics, University of Colorado Boulder, Boulder, CO, United States of America., Lester HA; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, United States of America.
المصدر: PloS one [PLoS One] 2017 Dec 05; Vol. 12 (12), pp. e0188715. Date of Electronic Publication: 2017 Dec 05 (Print Publication: 2017).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: GPI-Linked Proteins/*genetics , Receptors, Nicotinic/*physiology, Adaptor Proteins, Signal Transducing ; Animals ; Dopamine/metabolism ; HEK293 Cells ; Humans ; Mice ; Mice, Transgenic ; Neurons/metabolism ; RNA, Messenger/genetics
مستخلص: The α6 nicotinic acetylcholine receptor (nAChR) subunit is an attractive drug target for treating nicotine addiction because it is present at limited sites in the brain including the reward pathway. Lynx1 modulates several nAChR subtypes; lynx1-nAChR interaction sites could possibly provide drug targets. We found that dopaminergic cells from the substantia nigra pars compacta (SNc) express lynx1 mRNA transcripts and, as assessed by co-immunoprecipitation, α6 receptors form stable complexes with lynx1 protein, although co-transfection with lynx1 did not affect nicotine-induced currents from cell lines transfected with α6 and β2. To test whether lynx1 is important for the function of α6 nAChRs in vivo, we bred transgenic mice carrying a hypersensitive mutation in the α6 nAChR subunit (α6L9'S) with lynx1 knockout mice, providing a selective probe of the effects of lynx1 on α6* nAChRs. Lynx1 removal reduced the α6 component of nicotine-mediated rubidium efflux and dopamine (DA) release from synaptosomal preparations with no effect on numbers of α6β2 binding sites, indicating that lynx1 is functionally important for α6* nAChR activity. No effects of lynx1 removal were detected on nicotine-induced currents in slices from SNc, suggesting that lynx1 affects presynaptic α6* nAChR function more than somatic function. In the absence of agonist, lynx1 removal did not alter DA release in dorsal striatum as measured by fast scan cyclic voltammetry. Lynx1 removal affected some behaviors, including a novel-environment assay and nicotine-stimulated locomotion. Trends in 24-hour home-cage behavior were also suggestive of an effect of lynx1 removal. Conditioned place preference for nicotine was not affected by lynx1 removal. The results show that some functional and behavioral aspects of α6-nAChRs are modulated by lynx1.
References: Neuron. 1999 May;23(1):105-14. (PMID: 10402197)
Neuroscience. 2012 Jan 3;200:31-41. (PMID: 22079576)
J Pharmacol Exp Ther. 2011 Apr;337(1):187-200. (PMID: 21228066)
Proc Natl Acad Sci U S A. 2007 Feb 6;104(6):1983-8. (PMID: 17261803)
J Neurosci. 2009 Feb 18;29(7):2272-82. (PMID: 19228980)
J Neurochem. 2008 Jun;105(5):1861-72. (PMID: 18248617)
J Gen Physiol. 2014 Jan;143(1):51-66. (PMID: 24378908)
J Neurochem. 2013 Dec;127(6):762-71. (PMID: 23992036)
Biochem Pharmacol. 2007 Oct 15;74(8):1235-46. (PMID: 17825262)
J Neurosci. 2010 Jul 21;30(29):9877-89. (PMID: 20660270)
J Neurosci. 2007 Aug 1;27(31):8202-18. (PMID: 17670967)
J Neurosci. 2016 Sep 7;36(36):9472-8. (PMID: 27605620)
Neuropharmacology. 2007 Sep;53(3):390-405. (PMID: 17631923)
Biochem Pharmacol. 2011 Oct 15;82(8):828-41. (PMID: 21575611)
Neuropharmacology. 2000 Oct;39(13):2570-90. (PMID: 11044728)
Neurobiol Aging. 2016 Oct;46:13-21. (PMID: 27460145)
Biochem Pharmacol. 2013 Oct 15;86(8):1074-83. (PMID: 23939186)
J Pharmacol Exp Ther. 2009 Nov;331(2):547-54. (PMID: 19644040)
J Neurosci. 2010 Apr 14;30(15):5311-25. (PMID: 20392953)
J Neurosci. 2012 Jul 25;32(30):10226-37. (PMID: 22836257)
Nat Biotechnol. 2012 Aug;30(8):777-82. (PMID: 22820318)
Neuron. 2002 Mar 14;33(6):893-903. (PMID: 11906696)
J Neurosci. 2003 Aug 27;23(21):7820-9. (PMID: 12944511)
J Biol Chem. 2015 Oct 2;290(40):24509-18. (PMID: 26276394)
Science. 2010 Nov 26;330(6008):1238-40. (PMID: 21071629)
Biochem Pharmacol. 2011 Oct 15;82(8):862-72. (PMID: 21736871)
Curr Protoc Cytom. 2009 Apr;Chapter 12:Unit 12.15. (PMID: 19340807)
Neuron. 2006 Sep 7;51(5):587-600. (PMID: 16950157)
Cell Rep. 2017 Apr 25;19(4):688-696. (PMID: 28445721)
Mol Pharmacol. 2008 Jan;73(1):27-41. (PMID: 17932221)
Proc Natl Acad Sci U S A. 2001 Feb 27;98(5):2786-91. (PMID: 11226318)
J Biol Chem. 2013 May 31;288(22):15888-99. (PMID: 23585571)
Science. 2004 Nov 5;306(5698):1029-32. (PMID: 15528443)
Nicotine Tob Res. 2012 Nov;14(11):1258-69. (PMID: 22492084)
Neuropsychopharmacology. 2015 Jan;40(2):350-60. (PMID: 25035086)
J Neurosci. 2008 Nov 19;28(47):12318-27. (PMID: 19020025)
J Neurosci. 2014 Jul 16;34(29):9789-802. (PMID: 25031416)
J Biol Chem. 2011 Mar 25;286(12):10618-27. (PMID: 21252236)
Nat Protoc. 2012 Mar 01;7(3):562-78. (PMID: 22383036)
Neuropsychopharmacology. 2008 Aug;33(9):2158-66. (PMID: 18033235)
Biochem Pharmacol. 2011 Oct 15;82(8):873-82. (PMID: 21684266)
J Biol Chem. 2014 Nov 7;289(45):31423-32. (PMID: 25193667)
FASEB J. 2017 Apr;31(4):1398-1420. (PMID: 28100642)
Mol Pharmacol. 2000 May;57(5):913-25. (PMID: 10779374)
Biochem Pharmacol. 2011 Oct 15;82(8):852-61. (PMID: 21609715)
Genes Brain Behav. 2013 Jul;12(5):543-53. (PMID: 23594044)
Neuron. 2008 Oct 9;60(1):123-36. (PMID: 18940593)
J Neurochem. 2014 Apr;129(2):315-27. (PMID: 24266758)
Neuroscience. 2015 Jun 4;295:187-97. (PMID: 25813704)
Pharmacol Rev. 2012 Oct;64(4):869-79. (PMID: 22885704)
معلومات مُعتمدة: R01 DA003194 United States DA NIDA NIH HHS; R01 DA012242 United States DA NIDA NIH HHS; P30 DA015663 United States DA NIDA NIH HHS; R44 DA032464 United States DA NIDA NIH HHS; R01 DA017279 United States DA NIDA NIH HHS; R21 DA033831 United States DA NIDA NIH HHS; U19 DA019375 United States DA NIDA NIH HHS; R01 DA035942 United States DA NIDA NIH HHS; R41 DA032464 United States DA NIDA NIH HHS; R00 DA030396 United States DA NIDA NIH HHS; K99 DA030396 United States DA NIDA NIH HHS
المشرفين على المادة: 0 (Adaptor Proteins, Signal Transducing)
0 (GPI-Linked Proteins)
0 (LYNX1 protein, human)
0 (RNA, Messenger)
0 (Receptors, Nicotinic)
0 (nicotinic receptor alpha6)
VTD58H1Z2X (Dopamine)
تواريخ الأحداث: Date Created: 20171206 Date Completed: 20171229 Latest Revision: 20201214
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5716591
DOI: 10.1371/journal.pone.0188715
PMID: 29206881
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0188715