PMID- 28167133
OWN - NLM
STAT- MEDLINE
DCOM- 20180222
LR  - 20200930
IS  - 1873-2747 (Electronic)
IS  - 0361-9230 (Linking)
VI  - 130
DP  - 2017 Apr
TI  - NMDA receptor adjusted co-administration of ecstasy and cannabinoid receptor-1 
      agonist in the amygdala via stimulation of BDNF/Trk-B/CREB pathway in adult male 
      rats.
PG  - 221-230
LID - S0361-9230(16)30375-6 [pii]
LID - 10.1016/j.brainresbull.2017.01.020 [doi]
AB  - Consumption of cannabinoid receptor-1 (CB-1) agonist such as cannabis is widely 
      taken in 3,4- methylenedioxymethamphetamine (MDMA) or ecstasy users; it has been 
      hypothesized that co-consumption of CB-1 agonist might protect neurons against 
      MDMA toxicity. N-methyl-d-aspartate (NMDA) receptors regulate neuronal plasticity 
      and firing rate in the brain through Tyrosine-kinase B (Trk-B) activation. The 
      molecular and electrophysiological association among NMDA and 
      MDMA/Arachidonylcyclopropylamide (ACPA, a selective CB-1 receptor agonist) 
      co-consumption was not well-known. Here, neuronal spontaneous activity, 
      Brain-derived neurotrophic factor (BDNF), Trk-B and cAMP response element binding 
      protein (CREB) phosphorylation levels were recognized in ACPA and MDMA 
      co-injected rats. Besides, we proved the role of NMDA receptor on MDMA and ACPA 
      combination on neuronal spontaneous activity and Trk-B/BDNF pathway in the 
      central amygdala (CeA). Male rats were anesthetized with intra-peritoneal 
      injections of urethane; MDMA, D-2-amino-5-phosphonopentanoate (D-AP5, NMDA 
      receptor antagonist) were injected into CeA. ACPA was administrated by 
      intra-cerebroventricular injection. Thirty minutes following injections, neuronal 
      firing rate was recorded from CeA. Two hours after drug injection, amygdala was 
      collected from brain for molecular evaluations. Single administration of MDMA 
      and/or ACPA reduced firing rates compared with sham group in the CeA 
      dose-dependently. Injection of D-AP5, ACPA and MDMA reduced firing rate compared 
      with sham group (P<0.001). Interestingly, injection of ACPA+MDMA enhanced BDNF, 
      Trk-B and CREB phosphorylation compared with MDMA groups. D-AP5, ACPA and MDMA 
      co-injection decreased BDNF, Trk-B and CREB phosphorylation levels compared with 
      ACPA+MDMA in the amygdala (P<0.01). Probably, NMDA receptors are involved in the 
      protective role of acute MDMA+ACPA co-injection via BDNF/Trk-B/CREB pathways.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Ashabi, Ghorbangol
AU  - Ashabi G
AD  - Department of Physiology, Faculty of Medicine, Tehran University of Medical 
      Sciences, Tehran, Iran.
FAU - Sadat-Shirazi, Mitra-Sadat
AU  - Sadat-Shirazi MS
AD  - Iranian National Center for Addiction Studies (INCAS), Tehran University of 
      Medical Sciences, Tehran, Iran; Department of Neuroscience, School of Advanced 
      Technologies in Medicine, Tehran University of Medical Sciences, Tehran, Iran.
FAU - Khalifeh, Solmaz
AU  - Khalifeh S
AD  - Cognitive and Neuroscience Research Center (CNRC), Tehran Medical Sciences 
      Branch, Islamic Azad University, Tehran, Iran.
FAU - Elhampour, Laleh
AU  - Elhampour L
AD  - Iranian National Center for Addiction Studies (INCAS), Tehran University of 
      Medical Sciences, Tehran, Iran.
FAU - Zarrindast, Mohammad-Reza
AU  - Zarrindast MR
AD  - Iranian National Center for Addiction Studies (INCAS), Tehran University of 
      Medical Sciences, Tehran, Iran; Cognitive and Neuroscience Research Center 
      (CNRC), Tehran Medical Sciences Branch, Islamic Azad University, Tehran, Iran; 
      Institute for Cognitive Science Studies (ICSS), Tehran, Iran; Department of 
      Pharmacology, School of Medicine, Tehran University of Medical Sciences, Tehran, 
      Iran; Cognitive Sciences, Institute for Research in Fundamental Sciences (IPM), 
      Tehran, Iran; Medical Genomics Research Center, Tehran Medical Sciences Branch, 
      Islamic Azad University, Tehran, Iran. Electronic address: zarinmr@ams.ac.ir.
LA  - eng
PT  - Journal Article
DEP - 20170203
PL  - United States
TA  - Brain Res Bull
JT  - Brain research bulletin
JID - 7605818
RN  - 0 (Arachidonic Acids)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Cyclic AMP Response Element-Binding Protein)
RN  - 0 (Receptor, Cannabinoid, CB1)
RN  - 0 (Receptors, N-Methyl-D-Aspartate)
RN  - 0 (arachidonylcyclopropylamide)
RN  - EC 2.7.10.1 (Ntrk2 protein, rat)
RN  - EC 2.7.10.1 (Receptor, trkB)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Amygdala/*drug effects/*metabolism/physiology
MH  - Animals
MH  - Arachidonic Acids/administration & dosage
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Cyclic AMP Response Element-Binding Protein/metabolism
MH  - Male
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*administration & dosage
MH  - Neurons/drug effects/physiology
MH  - Phosphorylation
MH  - Rats, Wistar
MH  - Receptor, Cannabinoid, CB1/*agonists/*metabolism
MH  - Receptor, trkB/metabolism
MH  - Receptors, N-Methyl-D-Aspartate/*metabolism
MH  - Signal Transduction/*drug effects
OTO - NOTNLM
OT  - Amygdala
OT  - BDNF
OT  - CREB
OT  - Cannabinoid receptor-1
OT  - Ecstasy
OT  - NMDA receptor
EDAT- 2017/02/09 06:00
MHDA- 2018/02/23 06:00
CRDT- 2017/02/08 06:00
PHST- 2016/10/29 00:00 [received]
PHST- 2017/01/24 00:00 [revised]
PHST- 2017/01/27 00:00 [accepted]
PHST- 2017/02/09 06:00 [pubmed]
PHST- 2018/02/23 06:00 [medline]
PHST- 2017/02/08 06:00 [entrez]
AID - S0361-9230(16)30375-6 [pii]
AID - 10.1016/j.brainresbull.2017.01.020 [doi]
PST - ppublish
SO  - Brain Res Bull. 2017 Apr;130:221-230. doi: 10.1016/j.brainresbull.2017.01.020. 
      Epub 2017 Feb 3.