The D2-like Dopamine Receptor Agonist Quinpirole Microinjected Into the Ventral Pallidum Dose-Dependently Inhibits the VTA and Induces Place Aversion.


Journal

The international journal of neuropsychopharmacology
ISSN: 1469-5111
Titre abrégé: Int J Neuropsychopharmacol
Pays: England
ID NLM: 9815893

Informations de publication

Date de publication:
04 08 2022
Historique:
received: 28 01 2022
revised: 01 03 2022
accepted: 25 03 2022
pubmed: 30 3 2022
medline: 9 8 2022
entrez: 29 3 2022
Statut: ppublish

Résumé

The ventral pallidum (VP) is a dopaminoceptive forebrain structure regulating the ventral tegmental area (VTA) dopaminergic population activity. We have recently demonstrated that in the VP, the D2-like dopamine (DA) receptor agonist quinpirole dose dependently facilitates memory consolidation in inhibitory avoidance and spatial learning. According to our hypothesis, quinpirole microinjected into the VP can modulate the VTA DAergic activity and influence motivation and learning processes of rats. Quinpirole was microinjected at 3 different doses into the VP of male rats, and controls received vehicle. Single unit recordings were employed to assess VTA DAergic activity. To investigate the possible reinforcing or aversive effect of quinpirole in the VP, the conditioned place preference paradigm was used. Our results showed that intra-VP quinpirole microinjection regulates VTA DAergic neurons according to an inverted U-shaped dose-response curve. The largest dose of quinpirole decreased the population activity and strongly reduced burst activity of the DAergic neurons in the first hour after its application. In contrast, the 2 smaller doses increased DA population activity, but their effect started with a delay 1 hour after their microinjection. The CPP experiments revealed that the largest dose of quinpirole in the VP induced place aversion in the rats. Furthermore, the largest dose of quinpirole induced an acute locomotor activity reduction, while the medium dose led to a long-duration increase in locomotion. In summary, quinpirole dose dependently regulates VTA DAergic activity as well as the motivation and motor behavior of the rats at the level of the VP.

Sections du résumé

BACKGROUND
The ventral pallidum (VP) is a dopaminoceptive forebrain structure regulating the ventral tegmental area (VTA) dopaminergic population activity. We have recently demonstrated that in the VP, the D2-like dopamine (DA) receptor agonist quinpirole dose dependently facilitates memory consolidation in inhibitory avoidance and spatial learning. According to our hypothesis, quinpirole microinjected into the VP can modulate the VTA DAergic activity and influence motivation and learning processes of rats.
METHODS
Quinpirole was microinjected at 3 different doses into the VP of male rats, and controls received vehicle. Single unit recordings were employed to assess VTA DAergic activity. To investigate the possible reinforcing or aversive effect of quinpirole in the VP, the conditioned place preference paradigm was used.
RESULTS
Our results showed that intra-VP quinpirole microinjection regulates VTA DAergic neurons according to an inverted U-shaped dose-response curve. The largest dose of quinpirole decreased the population activity and strongly reduced burst activity of the DAergic neurons in the first hour after its application. In contrast, the 2 smaller doses increased DA population activity, but their effect started with a delay 1 hour after their microinjection. The CPP experiments revealed that the largest dose of quinpirole in the VP induced place aversion in the rats. Furthermore, the largest dose of quinpirole induced an acute locomotor activity reduction, while the medium dose led to a long-duration increase in locomotion.
CONCLUSIONS
In summary, quinpirole dose dependently regulates VTA DAergic activity as well as the motivation and motor behavior of the rats at the level of the VP.

Identifiants

pubmed: 35348731
pii: 6554836
doi: 10.1093/ijnp/pyac024
pmc: PMC9352176
doi:

Substances chimiques

Dopamine Agonists 0
Receptors, Dopamine D2 0
Quinpirole 20OP60125T

Types de publication

Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

590-599

Subventions

Organisme : NIMH NIH HHS
ID : R01 MH057440
Pays : United States
Organisme : NIMH NIH HHS
ID : R37 MH057440
Pays : United States

Informations de copyright

© The Author(s) 2022. Published by Oxford University Press on behalf of CINP.

Références

Neuron. 2005 Jun 2;46(5):703-13
pubmed: 15924857
Neuroscience. 1995 Feb;64(4):1045-55
pubmed: 7538637
Biol Psychiatry. 2014 Aug 1;76(3):223-30
pubmed: 24209776
J Neurosci Methods. 1989 Nov;30(2):141-6
pubmed: 2479799
Trends Neurosci. 2007 May;30(5):220-7
pubmed: 17400299
Brain Res. 1987 May;434(2):117-65
pubmed: 3107759
Synapse. 2002 Mar 1;43(3):151-62
pubmed: 11793420
Psychopharmacology (Berl). 1991;103(2):271-6
pubmed: 1674160
Cell Rep. 2016 Jun 21;15(12):2796-808
pubmed: 27292633
Eur J Neurosci. 2006 Nov;24(9):2429-38
pubmed: 17100831
Neurosci Biobehav Rev. 2018 Feb;85:1-20
pubmed: 28887225
J Neurosci. 2001 Jul 1;21(13):4915-22
pubmed: 11425919
Brain Res. 1996 Jan 22;707(1):64-74
pubmed: 8866714
Neuroscience. 1995 Feb;64(4):1019-34
pubmed: 7753373
Neuroscience. 1999;93(4):1349-58
pubmed: 10501459
Science. 2009 May 22;324(5930):1080-4
pubmed: 19389999
Prog Neurobiol. 2003 Apr;69(6):375-90
pubmed: 12880632
Trends Neurosci. 2012 Jul;35(7):422-30
pubmed: 22459161
Neuroscience. 2002;113(4):939-55
pubmed: 12182899
J Neurosci. 1984 Nov;4(11):2877-90
pubmed: 6150071
Neuron. 2021 Jul 7;109(13):2043-2044
pubmed: 34237276
J Neurosci. 2011 Mar 16;31(11):4280-9
pubmed: 21411669
J Neurochem. 2000 Feb;74(2):684-92
pubmed: 10646520
J Neurochem. 2001 Jun;77(5):1248-55
pubmed: 11389175
Proc Natl Acad Sci U S A. 1994 Nov 8;91(23):11271-5
pubmed: 7972046
Brain Res. 2003 Jun 20;976(1):30-40
pubmed: 12763619
Front Cell Neurosci. 2018 Aug 22;12:260
pubmed: 30186117
Brain Res. 1984 Mar 12;295(1):161-78
pubmed: 6201228
Behav Brain Res. 2016 Oct 15;313:1-9
pubmed: 27392640
Brain Res. 1993 Apr 23;609(1-2):71-80
pubmed: 8508323
eNeuro. 2018 May 16;5(2):
pubmed: 29780881
Behav Pharmacol. 1998 Jul;9(4):345-55
pubmed: 10065923
Neuroscience. 1994 Oct;62(4):1103-19
pubmed: 7845589
Brain Res. 1997 Apr 18;754(1-2):103-12
pubmed: 9134965
Drug Alcohol Depend. 2005 Mar 7;77(3):293-301
pubmed: 15734229
Behav Brain Res. 2017 Mar 15;321:99-105
pubmed: 28057528
Physiol Rev. 1998 Jan;78(1):189-225
pubmed: 9457173
Neuroreport. 1992 Jul;3(7):609-11
pubmed: 1421116
Neuron. 2021 Jul 7;109(13):2165-2182.e10
pubmed: 34048697
Neuroscience. 1992 Sep;50(2):371-86
pubmed: 1279461
Nat Neurosci. 2003 Sep;6(9):968-73
pubmed: 12897785
Proc Natl Acad Sci U S A. 2014 Apr 29;111(17):6455-60
pubmed: 24737889

Auteurs

Laszlo Peczely (L)

Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA.
Learning in Biological and Artificial Systems Research Group, Institute of Physiology, Pittsburgh, PA, USA.
Centre for Neuroscience, Pecs, Hungary.
University of Pecs, Pecs, Hungary.

Tamas Ollmann (T)

Learning in Biological and Artificial Systems Research Group, Institute of Physiology, Pittsburgh, PA, USA.
Neuropeptides, Cognition, Animal Models of Neuropsychiatric Disorders Research Group, Institute of Physiology, Pecs, Hungary.
Medical School, University of Pecs, Pecs, Hungary.
Centre for Neuroscience, Pecs, Hungary.
University of Pecs, Pecs, Hungary.

Kristof Laszlo (K)

Neuropeptides, Cognition, Animal Models of Neuropsychiatric Disorders Research Group, Institute of Physiology, Pecs, Hungary.
Medical School, University of Pecs, Pecs, Hungary.
Centre for Neuroscience, Pecs, Hungary.
University of Pecs, Pecs, Hungary.

Laszlo Lenard (L)

Learning in Biological and Artificial Systems Research Group, Institute of Physiology, Pittsburgh, PA, USA.
Molecular Neuroendocrinology and Neurophysiology Research Group, Szentagothai Research Centre, Pecs, Hungary.

Anthony A Grace (AA)

Departments of Neuroscience, Psychiatry and Psychology, University of Pittsburgh, Pittsburgh, PA, USA.

Articles similaires

Smoking Cessation and Incident Cardiovascular Disease.

Jun Hwan Cho, Seung Yong Shin, Hoseob Kim et al.
1.00
Humans Male Smoking Cessation Cardiovascular Diseases Female
Humans United States Aged Cross-Sectional Studies Medicare Part C
1.00
Humans Yoga Low Back Pain Female Male
Humans Meals Time Factors Female Adult

Classifications MeSH