PMID- 23508639
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20130320
LR  - 20220310
IS  - 2228-5806 (Print)
IS  - 2228-5814 (Electronic)
IS  - 2228-5806 (Linking)
VI  - 14
IP  - 3
DP  - 2012 Fall
TI  - The Role of The A2A Receptor in Cell Apoptosis Caused by MDMA.
PG  - 231-6
AB  - OBJECTIVE: Ecstasy, also known as 3, 4-methylenedioxymethamphetamine (MDMA), is a 
      psychoactive recreational hallucinogenic substance and a major worldwide 
      recreational drug. There are neurotoxic effects observed in laboratory animals 
      and humans following MDMA use. MDMA causes apoptosis in neurons of the central 
      nervous system (CNS). Withdrawal signs are attenuated by treatment with the 
      adenosine receptor (A2A receptor). This study reports the effects of glutamyl 
      cysteine synthetase (GCS), as an A2A receptor agonist, and succinylcholine (SCH), 
      as an A2A receptor antagonist, on Sprague Dawley rats, both in the presence and 
      absence of MDMA. MATERIALS AND METHODS: In this experimental study, we used seven 
      groups of Sprague Dawley rats (200-250 g each). Each group was treated with daily 
      intraperitoneal (IP) injections for a period of one week, as follows: i. MDMA (10 
      mg/kg); ii. GCS (0.3 mg/kg); iii. SCH (0.3 mg/kg); iv. GCS + SCH (0.3 mg/kg 
      each); v. MDMA (10 mg/kg) + GCS (0.3 mg/kg); vi. MDMA (10 mg/kg) + SCH (0.3 
      mg/kg); and vi. normal saline (1 cc/kg) as the sham group. Bax (apoptotic 
      protein) and Bcl-2 (anti-apoptotic protein) expressions were evaluated by 
      striatum using RT-PCR and Western blot analysis. RESULTS: There was a significant 
      increase in Bax protein expression in the MDMA+SCH group and a significant 
      decrease in Bcl-2 protein expression in the MDMA+SCH group (p<0.05). CONCLUSION: 
      A2A receptors have a role in the apoptotic effects of MDMA via the Bax and Bcl-2 
      pathways. An agonist of this receptor (GCS) decreases the cytotoxcity of MDMA, 
      while the antagonist of this receptor (SCH) increases its cytotoxcity.
FAU - Soleimani, Mansooreh
AU  - Soleimani M
AD  - 1. Cellular and Molecular Research Center, Tehran University of Medical Sciences, 
      Tehran, Iran.
FAU - Katebi, Majid
AU  - Katebi M
FAU - Alizadeh, Akram
AU  - Alizadeh A
FAU - Mohammadzadeh, Farzaneh
AU  - Mohammadzadeh F
FAU - Mehdizadeh, Mehdi
AU  - Mehdizadeh M
LA  - eng
PT  - Journal Article
DEP - 20121212
PL  - Iran
TA  - Cell J
JT  - Cell journal
JID - 101566618
PMC - PMC3584434
OTO - NOTNLM
OT  - Adenosine Receptor
OT  - Agonist of A2A Receptor
OT  - Antagonist of A2A Receptor
OT  - Ecstasy or MDMA
OT  - Neurotoxicity
EDAT- 2013/03/20 06:00
MHDA- 2013/03/20 06:01
PMCR- 2012/09/01
CRDT- 2013/03/20 06:00
PHST- 2011/12/29 00:00 [received]
PHST- 2012/04/28 00:00 [accepted]
PHST- 2013/03/20 06:00 [entrez]
PHST- 2013/03/20 06:00 [pubmed]
PHST- 2013/03/20 06:01 [medline]
PHST- 2012/09/01 00:00 [pmc-release]
PST - ppublish
SO  - Cell J. 2012 Fall;14(3):231-6. Epub 2012 Dec 12.