PMID- 23276666
OWN - NLM
STAT- MEDLINE
DCOM- 20130822
LR  - 20211021
IS  - 1879-0712 (Electronic)
IS  - 0014-2999 (Print)
IS  - 0014-2999 (Linking)
VI  - 701
IP  - 1-3
DP  - 2013 Feb 15
TI  - Effects of a short-course MDMA binge on dopamine transporter binding and on 
      levels of dopamine and its metabolites in adult male rats.
PG  - 176-80
LID - S0014-2999(12)01041-2 [pii]
LID - 10.1016/j.ejphar.2012.12.024 [doi]
AB  - Although the recreational drug 3,4-methylenedioxymethamphetamine (MDMA) is often 
      described as a selective serotonergic neurotoxin, some research has challenged 
      this view. The objective of this study was to determine the influence of MDMA on 
      subsequent levels of two different markers of dopaminergic function, the dopamine 
      transporter (DAT) as well as dopamine and its major metabolites. In experiment I, 
      adult male Sprague-Dawley rats were administered either a low or moderate dose 
      MDMA binge (2.5 or 5.0mg/kgx4 with an inter-dose interval of 1h) or saline, and 
      were killed 1 week later. The moderate dose dramatically reduced [(3)H]WIN 35,428 
      binding to striatal DAT by 73.7% (P</=0.001). In experiment II, animals were binged 
      with a higher dose of MDMA (10mg/kgx4) to determine the drug's effects on 
      concentrations of serotonin (5-HT), dopamine, and their respective major 
      metabolites 5-hydroxyindoleacetic acid (5-HIAA), dihydroxyphenylacetic acid 
      (DOPAC), and homovanillic acid (HVA) in the striatum and frontal cortex 1 week 
      later. As expected, MDMA significantly reduced 5-HT and 5-HIAA (>/=50%) in these 
      structures, while only a marginal decrease in dopamine was noted in the striatum. 
      In contrast, levels of DOPAC (34.3%, P<0.01) and HVA (33.5%, P<0.001) were 
      reduced by MDMA treatment, suggesting a decrease in dopamine turnover. Overall, 
      these findings indicate that while serotonergic markers are particularly 
      vulnerable to MDMA-induced depletion, significant dopaminergic deficits may also 
      occur under some conditions. Importantly, DAT expression may be more vulnerable 
      to perturbation by MDMA than dopamine itself.
CI  - Copyright (c) 2012 Elsevier B.V. All rights reserved.
FAU - Biezonski, Dominik K
AU  - Biezonski DK
AD  - Neuroscience and Behavior Program, University of Massachusetts, Amherst, MA 
      01003, USA.
FAU - Piper, Brian J
AU  - Piper BJ
FAU - Shinday, Nina M
AU  - Shinday NM
FAU - Kim, Peter J
AU  - Kim PJ
FAU - Ali, Syed F
AU  - Ali SF
FAU - Meyer, Jerrold S
AU  - Meyer JS
LA  - eng
GR  - L30 DA027582/DA/NIDA NIH HHS/United States
GR  - L30DA027582/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20121228
PL  - Netherlands
TA  - Eur J Pharmacol
JT  - European journal of pharmacology
JID - 1254354
RN  - 0 (Dopamine Plasma Membrane Transport Proteins)
RN  - 333DO1RDJY (Serotonin)
RN  - 54-16-0 (Hydroxyindoleacetic Acid)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Dopamine/*metabolism
MH  - Dopamine Plasma Membrane Transport Proteins/*metabolism
MH  - Hydroxyindoleacetic Acid/metabolism
MH  - Male
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*pharmacology
MH  - Protein Binding/drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Serotonin/metabolism
MH  - Time Factors
PMC - PMC3664040
MID - NIHMS432288
EDAT- 2013/01/02 06:00
MHDA- 2013/08/24 06:00
PMCR- 2014/02/15
CRDT- 2013/01/02 06:00
PHST- 2012/06/08 00:00 [received]
PHST- 2012/12/05 00:00 [revised]
PHST- 2012/12/18 00:00 [accepted]
PHST- 2013/01/02 06:00 [entrez]
PHST- 2013/01/02 06:00 [pubmed]
PHST- 2013/08/24 06:00 [medline]
PHST- 2014/02/15 00:00 [pmc-release]
AID - S0014-2999(12)01041-2 [pii]
AID - 10.1016/j.ejphar.2012.12.024 [doi]
PST - ppublish
SO  - Eur J Pharmacol. 2013 Feb 15;701(1-3):176-80. doi: 10.1016/j.ejphar.2012.12.024. 
      Epub 2012 Dec 28.