Cocaine hydrolase blocks cocaine-induced dopamine transporter trafficking to the plasma membrane.
Animals
Carboxylic Ester Hydrolases
/ metabolism
Cell Membrane
/ drug effects
Cocaine
/ pharmacology
Cocaine-Related Disorders
Dopamine Plasma Membrane Transport Proteins
/ drug effects
Dose-Response Relationship, Drug
Hyperkinesis
/ pathology
Male
Rats
Rats, Sprague-Dawley
Recombinant Proteins
/ metabolism
addiction
brain
dopamine transporter
hydrolase
trafficking
Journal
Addiction biology
ISSN: 1369-1600
Titre abrégé: Addict Biol
Pays: United States
ID NLM: 9604935
Informations de publication
Date de publication:
01 2022
01 2022
Historique:
revised:
21
07
2021
received:
01
05
2021
accepted:
27
07
2021
pubmed:
8
8
2021
medline:
23
2
2022
entrez:
7
8
2021
Statut:
ppublish
Résumé
Cocaine blocks dopamine uptake via dopamine transporter (DAT) on plasma membrane of neuron cells and, as a result, produces the high and induces DAT trafficking to plasma membrane which contributes to the drug seeking or craving. In this study, we first examined the dose dependence of cocaine-induced DAT trafficking and hyperactivity in rats, demonstrating that cocaine at an intraperitoneal dose of 10 mg/kg or higher led to redistribution of most DAT to the plasma membrane while inducing significant hyperactivity in rats. However, administration of 5-mg/kg cocaine (ip) did not significantly induce DAT trafficking or hyperactivity in rats. So the threshold (intraperitoneal) dose of cocaine that can significantly induce DAT trafficking or hyperactivity should be between 5 and 10 mg/kg. These data suggest that when a cocaine dose is high enough to induce significant hyperactivity, it can also significantly induce DAT trafficking to the plasma membrane. Further, the threshold brain cocaine concentration required to induce significant hyperactivity and DAT trafficking was estimated to be ~2.0 ± 0.8 μg/g. Particularly, for treatment of cocaine abuse, previous studies demonstrated that an exogenous cocaine-metabolizing enzyme, for example, CocH3-Fc(M3), can effectively block cocaine-induced hyperactivity. However, it was unknown whether an enzyme could also effectively block cocaine-induced DAT trafficking to the plasma membrane. This study demonstrates, for the first time, that the enzyme is also capable of effectively blocking cocaine from reaching the brain even with a lethal dose of 60-mg/kg cocaine (ip) and, thus, powerfully preventing cocaine-induced physiological effects such as the hyperactivity and DAT trafficking.
Identifiants
pubmed: 34363291
doi: 10.1111/adb.13089
pmc: PMC8720053
mid: NIHMS1728776
doi:
Substances chimiques
Dopamine Plasma Membrane Transport Proteins
0
Recombinant Proteins
0
Carboxylic Ester Hydrolases
EC 3.1.1.-
cocaine hydrolase
EC 3.1.1.8
Cocaine
I5Y540LHVR
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
e13089Subventions
Organisme : NIDA NIH HHS
ID : R01 DA035552
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA032910
Pays : United States
Organisme : NIDA NIH HHS
ID : UH2 DA041115
Pays : United States
Organisme : NIDA NIH HHS
ID : UH3 DA041115
Pays : United States
Organisme : NIDA NIH HHS
ID : U18 DA052319
Pays : United States
Organisme : NIDA NIH HHS
ID : U01 DA051079
Pays : United States
Organisme : NIDA NIH HHS
ID : R01 DA013930
Pays : United States
Informations de copyright
© 2021 Society for the Study of Addiction.
Références
Chem Biol Interact. 2019 Jun 1;306:89-95
pubmed: 30986387
J Neurosci. 2009 Mar 11;29(10):3328-36
pubmed: 19279270
Drug Alcohol Depend. 2019 Nov 1;204:107462
pubmed: 31499241
Neuropharmacology. 2020 Oct 1;176:108251
pubmed: 32710979
Neuropsychopharmacology. 2009 Apr;34(5):1162-71
pubmed: 18769473
Biophys J. 2007 Nov 15;93(10):3627-39
pubmed: 17704152
Proc Natl Acad Sci U S A. 2016 Jan 12;113(2):422-7
pubmed: 26712009
AAPS J. 2017 Nov 27;20(1):3
pubmed: 29181644
Open Pharmacol J. 2008;2(9):70-78
pubmed: 19568322
Science. 1987 Sep 4;237(4819):1219-23
pubmed: 2820058
Future Med Chem. 2011 Jan;3(1):9-13
pubmed: 21428822
Ann N Y Acad Sci. 2010 Feb;1187:316-40
pubmed: 20201860
Mol Pharmacol. 2011 Feb;79(2):290-7
pubmed: 20971807
J Am Chem Soc. 2008 Sep 10;130(36):12148-55
pubmed: 18710224
Biochem J. 2014 Jun 15;460(3):447-57
pubmed: 24870023
ACS Chem Biol. 2016 Aug 19;11(8):2186-94
pubmed: 27224254
J Biol Chem. 1997 Jun 13;272(24):15541-6
pubmed: 9182590
Proc Natl Acad Sci U S A. 2005 Nov 15;102(46):16656-61
pubmed: 16275916
J Pharmacol Exp Ther. 2013 Nov;347(2):251-7
pubmed: 23978563
Sci Rep. 2017 Nov 10;7(1):15303
pubmed: 29127295
AAPS J. 2018 Mar 19;20(3):53
pubmed: 29556863
Neuropharmacology. 2005 Nov;49(6):750-8
pubmed: 16212991
Future Med Chem. 2009 Jun;1(3):515-28
pubmed: 20161378
Mol Pharmacol. 2002 Feb;61(2):436-45
pubmed: 11809869
J Biol Chem. 1994 Apr 22;269(16):12290-7
pubmed: 8163533
Neurobiol Aging. 2003 Dec;24(8):1147-54
pubmed: 14643386
Nat Commun. 2014 Mar 18;5:3457
pubmed: 24643289
Biochem J. 2014 Jan 1;457(1):197-206
pubmed: 24125115
J Phys Chem B. 2009 Nov 12;113(45):15057-66
pubmed: 19831380
Neuropsychopharmacology. 2013 Dec;38(13):2588-97
pubmed: 23822950
Org Biomol Chem. 2008 Mar 7;6(5):836-43
pubmed: 18292872
Nat Rev Neurosci. 2003 Jan;4(1):13-25
pubmed: 12511858
Front Neural Circuits. 2013 Oct 11;7:152
pubmed: 24130517
J Comput Aided Mol Des. 2008 Sep;22(9):661-71
pubmed: 17989928
J Pharm Biomed Anal. 2017 Feb 5;134:243-251
pubmed: 27923200
Pharmacol Biochem Behav. 2017 Aug;159:69-75
pubmed: 28712749
AAPS J. 2020 Mar 18;22(3):62
pubmed: 32189158
Psychopharmacology (Berl). 2005 Oct;182(2):245-52
pubmed: 16001116
Pharmacol Ther. 2004 Oct;104(1):17-27
pubmed: 15500906
J Cell Sci. 1999 Oct;112 ( Pt 20):3559-67
pubmed: 10504304
J Neurosci. 2015 Sep 16;35(37):12845-58
pubmed: 26377471
Org Biomol Chem. 2013 Nov 21;11(43):7477-85
pubmed: 24077614
Pharmacol Rev. 2011 Sep;63(3):585-640
pubmed: 21752877
Bioorg Med Chem. 2014 Jan 1;22(1):538-49
pubmed: 24290065
Future Med Chem. 2012 Feb;4(2):125-8
pubmed: 22300091