PMID- 22916213
OWN - NLM
STAT- MEDLINE
DCOM- 20130116
LR  - 20211021
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 7
IP  - 8
DP  - 2012
TI  - Role of the dopaminergic system in the acquisition, expression and reinstatement 
      of MDMA-induced conditioned place preference in adolescent mice.
PG  - e43107
LID - 10.1371/journal.pone.0043107 [doi]
LID - e43107
AB  - BACKGROUND: The rewarding effects of 3,4-methylenedioxy-metamphetamine (MDMA) 
      have been demonstrated in conditioned place preference (CPP) procedures, but the 
      involvement of the dopaminergic system in MDMA-induced CPP and reinstatement is 
      poorly understood. METHODOLOGY/PRINCIPAL FINDINGS: In this study, the effects of 
      the DA D1 antagonist SCH 23390 (0.125 and 0.250 mg/kg), the DA D2 antagonist 
      Haloperidol (0.1 and 0.2 mg/kg), the D2 antagonist Raclopride (0.3 and 0.6 mg/kg) 
      and the dopamine release inhibitor CGS 10746B (3 and 10 mg/kg) on the 
      acquisition, expression and reinstatement of a CPP induced by 10 mg/kg of MDMA 
      were evaluated in adolescent mice. As expected, MDMA significantly increased the 
      time spent in the drug-paired compartment during the post-conditioning (Post-C) 
      test, and a priming dose of 5 mg/kg reinstated the extinguished preference. The 
      higher doses of Haloperidol, Raclopride and CGS 10746B and both doses of SCH 
      23390 blocked acquisition of the MDMA-induced CPP. However, only Haloperidol 
      blocked expression of the CPP. Reinstatement of the extinguished preference was 
      not affected by any of the drugs studied. Analysis of brain monoamines revealed 
      that the blockade of CPP acquisition was accompanied by an increase in DA 
      concentration in the striatum, with a concomitant decrease in DOPAC and HVA 
      levels. Administration of haloperidol during the Post-C test produced increases 
      in striatal serotonin, DOPAC and HVA concentrations. In mice treated with the 
      higher doses of haloperidol and CGS an increase in SERT concentration in the 
      striatum was detected during acquisition of the CPP, but no changes in DAT were 
      observed. CONCLUSIONS/SIGNIFICANCE: These results demonstrate that, in adolescent 
      mice, the dopaminergic system is involved in the acquisition and expression of 
      MDMA-induced CPP, but not in its reinstatement.
FAU - Vidal-Infer, Antonio
AU  - Vidal-Infer A
AD  - Unit of Research on Psychobiology of Drug Dependence, University of Valencia, 
      Valencia, Spain.
FAU - Roger-Sanchez, Concepcion
AU  - Roger-Sanchez C
FAU - Daza-Losada, Manuel
AU  - Daza-Losada M
FAU - Aguilar, Maria A
AU  - Aguilar MA
FAU - Minarro, Jose
AU  - Minarro J
FAU - Rodriguez-Arias, Marta
AU  - Rodriguez-Arias M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120816
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Benzazepines)
RN  - 0 (Dopamine Antagonists)
RN  - 0 (SCH 23390)
RN  - 0 (Thiazepines)
RN  - 333DO1RDJY (Serotonin)
RN  - 430K3SOZ7G (Raclopride)
RN  - 81382-52-7 (CGS 10746B)
RN  - J6292F8L3D (Haloperidol)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Benzazepines/pharmacology
MH  - Blotting, Western
MH  - Conditioning, Operant/*drug effects
MH  - Dopamine/*metabolism
MH  - Dopamine Antagonists/pharmacology
MH  - Haloperidol/pharmacology
MH  - Male
MH  - Mice
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*pharmacology
MH  - Raclopride/pharmacology
MH  - Serotonin/metabolism
MH  - Thiazepines/pharmacology
PMC - PMC3420895
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2012/08/24 06:00
MHDA- 2013/01/17 06:00
PMCR- 2012/08/16
CRDT- 2012/08/24 06:00
PHST- 2011/11/21 00:00 [received]
PHST- 2012/07/19 00:00 [accepted]
PHST- 2012/08/24 06:00 [entrez]
PHST- 2012/08/24 06:00 [pubmed]
PHST- 2013/01/17 06:00 [medline]
PHST- 2012/08/16 00:00 [pmc-release]
AID - PONE-D-11-23518 [pii]
AID - 10.1371/journal.pone.0043107 [doi]
PST - ppublish
SO  - PLoS One. 2012;7(8):e43107. doi: 10.1371/journal.pone.0043107. Epub 2012 Aug 16.