PMID- 23212481
OWN - NLM
STAT- MEDLINE
DCOM- 20130802
LR  - 20220310
IS  - 1573-7365 (Electronic)
IS  - 0885-7490 (Linking)
VI  - 28
IP  - 1
DP  - 2013 Mar
TI  - Effects of adenosine A2a receptor agonist and antagonist on hippocampal nuclear 
      factor-kB expression preceded by MDMA toxicity.
PG  - 45-52
LID - 10.1007/s11011-012-9366-y [doi]
AB  - There is an abundance of evidence showing that repeated use of 
      3,4-methlylenedioxymethamphetamine (MDMA; ecstasy) is associated with brain 
      dysfunction, memory disturbance, locomotor hyperactivity, and hyperthermia. MDMA 
      is toxic to both the serotonergic neurons and dopaminergic system. Adenosine is 
      an endogenous purine nucleoside with a neuromodulatory function in the central 
      nervous system. Nuclear factor kappa-B (NF-kB) plays a pivotal role in the 
      initiation and perpetuation of an immune response by triggering the expression of 
      major inflammatory mediators such as cytokines, chemokines, and adhesion 
      molecules. Here, we investigated the effects of the A2a adenosine receptor 
      (A2a-R) agonist (CGS) and antagonist (SCH) on NF-kB expression after MDMA 
      administration. Male Sprague-Dawley rats were injected to MDMA (10 mg/kg) 
      followed by intraperitoneal injection of either CGS or SCH (0.03 mg/kg each) to 
      animals. The hippocampi were then removed for western blot and RT- PCR analyses. 
      MDMA significantly elevated NF-kB expression. Our results show that 
      administration of CGS following MDMA significantly elevated the NF-kB expression 
      both at mRNA and protein levels. By contrast, administration of the A2a-R 
      antagonist SCH resulted in a decrease in the NF-kB levels. Taken together, these 
      results indicate that, co-administration of A2a agonist (CGS) can protect against 
      MDMA neurotoxic effects by increasing NF-kB expression levels; suggesting a 
      potential application for protection against the neurotoxic effects observed in 
      MDMA users.
FAU - Kermanian, Fatemeh
AU  - Kermanian F
AD  - Department of Anatomy and Cell Biology, School of Medicine, Mashhad University of 
      Medical Sciences, Mashhad, Iran. kermanian_s@yahoo.com
FAU - Soleimani, Mansooreh
AU  - Soleimani M
FAU - Ebrahimzadeh, Alireza
AU  - Ebrahimzadeh A
FAU - Haghir, Hossein
AU  - Haghir H
FAU - Mehdizadeh, Mehdi
AU  - Mehdizadeh M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20121206
PL  - United States
TA  - Metab Brain Dis
JT  - Metabolic brain disease
JID - 8610370
RN  - 0 (Adenosine A2 Receptor Agonists)
RN  - 0 (Adenosine A2 Receptor Antagonists)
RN  - 0 (NF-kappa B)
RN  - 0 (Receptor, Adenosine A2A)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Adenosine A2 Receptor Agonists/*pharmacology
MH  - Adenosine A2 Receptor Antagonists/*pharmacology
MH  - Animals
MH  - Hippocampus/*metabolism
MH  - Male
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*toxicity
MH  - NF-kappa B/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptor, Adenosine A2A/physiology
EDAT- 2012/12/06 06:00
MHDA- 2013/08/03 06:00
CRDT- 2012/12/06 06:00
PHST- 2012/09/10 00:00 [received]
PHST- 2012/11/22 00:00 [accepted]
PHST- 2012/12/06 06:00 [entrez]
PHST- 2012/12/06 06:00 [pubmed]
PHST- 2013/08/03 06:00 [medline]
AID - 10.1007/s11011-012-9366-y [doi]
PST - ppublish
SO  - Metab Brain Dis. 2013 Mar;28(1):45-52. doi: 10.1007/s11011-012-9366-y. Epub 2012 
      Dec 6.