Involvement of Basolateral Amygdala Dopamine D1 Receptors in the Acquisition and Expression of Morphine-Induced Place Preference in Rats.

Addiction basolateral amygdala dopamine-D1 receptor morphine

Journal

Advanced biomedical research
ISSN: 2277-9175
Titre abrégé: Adv Biomed Res
Pays: India
ID NLM: 101586897

Informations de publication

Date de publication:
2022
Historique:
received: 08 09 2021
revised: 01 11 2021
accepted: 08 11 2021
entrez: 14 3 2022
pubmed: 15 3 2022
medline: 15 3 2022
Statut: epublish

Résumé

In the present study, the effects of intra-basolateral amygdala (BLA) blockade of dopamine D1 receptor on morphine-induced conditioned place preference (CPP) were investigated in male Wistar rats. A 5-day CPP paradigm was used. Morphine was injected subsequently at effective (5 mg/kg) and ineffective (0.5 mg/kg) doses. SCH 23390 (0.5- μg/rat), as a selective D1 receptor antagonist, was microinjected bilaterally into the BLA. Effective dose of morphine induced a significant CPP, and increased the locomotor activity during the testing phase. The results showed that morphine-induced CPP was significantly suppressed by D1 receptors antagonist in BLA in the acquisition phase and caused an aversion even at high doses. The antagonist also significantly prevented CPP expression. Morphine increased the motor activity, but the D1 receptors blockade, significantly reduced it. The findings of this study suggest a possible role for BLA dopamine D1 receptors in reward responses in morphine dependency.

Sections du résumé

Background UNASSIGNED
In the present study, the effects of intra-basolateral amygdala (BLA) blockade of dopamine D1 receptor on morphine-induced conditioned place preference (CPP) were investigated in male Wistar rats.
Materials and Methods UNASSIGNED
A 5-day CPP paradigm was used. Morphine was injected subsequently at effective (5 mg/kg) and ineffective (0.5 mg/kg) doses. SCH 23390 (0.5- μg/rat), as a selective D1 receptor antagonist, was microinjected bilaterally into the BLA.
Results UNASSIGNED
Effective dose of morphine induced a significant CPP, and increased the locomotor activity during the testing phase. The results showed that morphine-induced CPP was significantly suppressed by D1 receptors antagonist in BLA in the acquisition phase and caused an aversion even at high doses. The antagonist also significantly prevented CPP expression. Morphine increased the motor activity, but the D1 receptors blockade, significantly reduced it.
Conclusions UNASSIGNED
The findings of this study suggest a possible role for BLA dopamine D1 receptors in reward responses in morphine dependency.

Identifiants

pubmed: 35284350
doi: 10.4103/abr.abr_284_21
pii: ABR-11-8
pmc: PMC8906092
doi:

Types de publication

Journal Article

Langues

eng

Pagination

8

Informations de copyright

Copyright: © 2022 Advanced Biomedical Research.

Déclaration de conflit d'intérêts

There are no conflicts of interest.

Références

Behav Brain Res. 2016 Oct 1;312:394-404
pubmed: 27374160
Drug Alcohol Rev. 2014 Jan;33(1):19-26
pubmed: 24261474
Psychopharmacology (Berl). 1999 Aug;145(3):237-50
pubmed: 10494572
Brain Res. 1991 Jun 21;552(1):141-52
pubmed: 1833032
Int J Mol Sci. 2019 Sep 03;20(17):
pubmed: 31484312
J Neurosci. 2011 Aug 3;31(31):11172-83
pubmed: 21813678
Neuroscience. 2005;135(2):335-45
pubmed: 16111818
Pharmacol Biochem Behav. 2000 Jun;66(2):285-92
pubmed: 10880680
J Neurochem. 2016 Dec;139(6):1071-1080
pubmed: 27546491
Neuropharmacology. 1986 Nov;25(11):1297-300
pubmed: 2948132
Neurosci Biobehav Rev. 2015 Oct;57:271-83
pubmed: 26341938
Eur J Neurosci. 2013 Mar;37(6):972-81
pubmed: 23320810
J Med Chem. 1992 Feb 7;35(3):502-7
pubmed: 1531365
Psychopharmacology (Berl). 1991;103(2):209-14
pubmed: 1827526
Hippocampus. 1996;6(5):495-512
pubmed: 8953303
J Neurosci. 2018 Jul 11;38(28):6340-6349
pubmed: 29941444
Mol Neurobiol. 2019 Oct;56(10):6756-6769
pubmed: 30919214
J Neurosci. 1999 Dec 15;19(24):11027-39
pubmed: 10594083
Behav Brain Res. 2009 Mar 17;198(2):466-71
pubmed: 19073220
Neurosci Lett. 2013 Apr 29;541:138-43
pubmed: 23499959
J Neural Transm Suppl. 1993;40:1-12
pubmed: 7905022
Neurobiol Learn Mem. 2014 Feb;108:28-37
pubmed: 23742917
Surg Neurol. 2001 Feb;55(2):79-86; discussion 86-8
pubmed: 11301086
ACS Pharmacol Transl Sci. 2019 Feb 8;2(1):52-65
pubmed: 30775693
Synapse. 1998 Oct;30(2):181-93
pubmed: 9723788
J Neurosci. 1991 Jul;11(7):2107-16
pubmed: 2066777
Behav Brain Res. 2012 May 16;231(1):111-5
pubmed: 22426507
J Womens Health (Larchmt). 2015 Aug;24(8):629-35
pubmed: 26153668
Nature. 1990 Sep 6;347(6288):72-6
pubmed: 2144334
J Comp Physiol Psychol. 1981 Apr;95(2):351-62
pubmed: 6262390
Neuron. 2012 Oct 4;76(1):33-50
pubmed: 23040805
J Neurosci. 1996 Aug 15;16(16):5256-65
pubmed: 8756453
Cells. 2021 Mar 26;10(4):
pubmed: 33810328
Proc Natl Acad Sci U S A. 1991 Oct 15;88(20):9175-9
pubmed: 1833775
Neuron. 2018 Jan 17;97(2):434-449.e4
pubmed: 29307710
Psychopharmacology (Berl). 2003 Jul;168(1-2):124-131
pubmed: 12607074
Prog Neurobiol. 1980;14(2-3):69-97
pubmed: 6999537
Behav Neurosci. 1993 Feb;107(1):3-22
pubmed: 8447956
J Psychopharmacol. 2013 Feb;27(2):181-91
pubmed: 23151613
J Pharmacol Exp Ther. 2000 Aug;294(2):680-7
pubmed: 10900248
Neuron. 2008 Aug 28;59(4):648-61
pubmed: 18760700
J Neurosci. 1990 Jun;10(6):1906-11
pubmed: 2355257
Exp Mol Med. 2018 Apr 9;50(4):1-16
pubmed: 29628509
Nature. 1991 Apr 18;350(6319):610-4
pubmed: 1840645
Neuron. 2012 Nov 21;76(4):790-803
pubmed: 23177963
J Neurosci. 2002 May 1;22(9):3312-20
pubmed: 11978805
J Neurosci. 2001 Aug 15;21(16):6370-6
pubmed: 11487660
Nature. 2001 Jul 5;412(6842):43-8
pubmed: 11452299
Behav Pharmacol. 2001 Dec;12(8):603-11
pubmed: 11856897
J Psychopharmacol. 2003 Dec;17(4):415-23
pubmed: 14870954
Brain Res. 2003 Mar 7;965(1-2):212-21
pubmed: 12591140

Auteurs

Zahra Rezaei (Z)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Hojjatallah Alaei (H)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Parham Reisi (P)

Department of Physiology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Classifications MeSH