PMID- 26735788
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20160108
LR  - 20160107
IS  - 1355-6215 (Print)
IS  - 1355-6215 (Linking)
VI  - 2
IP  - 3
DP  - 1997 Jul
TI  - Induction of Fos protein by 3,4- methylenedioxymethamphetamine (Ecstasy) in rat 
      brain: regional differences in pharmacological manipulation.
PG  - 317-26
LID - 10.1080/13556219772615 [doi]
AB  - Psychostimulant drugs have been reported to increase the expression of some 
      immediate-early genes in the brain. In the present study, immunohistochemical 
      techniques were used to assess the pattern of Fos protein produced by 
      3,4-methylenedioxymethamphetamine (MDMA) in several brain regions. Furthermore, 
      we also studied the role of the dopamine D and D receptors and the N-methyl- 
      D-aspartate (NMDA) receptor in the induction of Fos protein by MDMA. A single 
      administration of MDMA (5, 10 or 20 mg/kg) caused marked induction of 
      Fos-immunoreactivity in several regions including frontal cortex, striatum and 
      olfactory tubercle of rat brain, in a dose-dependent manner. However, in the 
      hippocampus and cerebellum, there were few or no Fos immunoreactive cells induced 
      by MDMA. Furthermore, the induction of Fos protein in the striatum and olfactory 
      tubercle after administration of MDMA (10 mg/kg) was blocked by pre-treatment 
      with the dopamine D receptor antagonist SCH 23390 (1 mg/kg) or the NMDA receptor 
      antagonist dizocilpine (1 mg/kg), but not by the dopamine D receptor antagonist 
      (-)-sulpiride (100 mg/kg). However, the induction of Fos protein in the frontal 
      cortex and hippocampus by MDMA was unaltered by pretreatment with SCH 23390 (1 
      mg/kg) or (-)-sulpiride (100 mg/kg). These results suggest that MDMA induces the 
      expression of Fos protein in several regions of rat brain, and that the 
      expression of Fos protein by MDMA in the striatum and olfactory tubercle appears 
      to be mediated at least in part by the dopamine D and NMDA receptors.
FAU - Hashimoto, K
AU  - Hashimoto K
AD  - Division of Cortical Function Disorders, National Institute of Neuroscience, 
      National Center of Neurology and Psychiatry, Tokyo.Division of Drug Dependence 
      and Psychotropic Drug Clinical Research, National Institute of Mental Health, 
      Chiba, Japan.
FAU - Tomitaka, S
AU  - Tomitaka S
AD  - Division of Cortical Function Disorders, National Institute of Neuroscience, 
      National Center of Neurology and Psychiatry, Tokyo.Division of Drug Dependence 
      and Psychotropic Drug Clinical Research, National Institute of Mental Health, 
      Chiba, Japan.
FAU - Narita, N
AU  - Narita N
AD  - Division of Cortical Function Disorders, National Institute of Neuroscience, 
      National Center of Neurology and Psychiatry, Tokyo.Division of Drug Dependence 
      and Psychotropic Drug Clinical Research, National Institute of Mental Health, 
      Chiba, Japan.
FAU - Minabe, Y
AU  - Minabe Y
AD  - Division of Cortical Function Disorders, National Institute of Neuroscience, 
      National Center of Neurology and Psychiatry, Tokyo.Division of Drug Dependence 
      and Psychotropic Drug Clinical Research, National Institute of Mental Health, 
      Chiba, Japan.
FAU - Iyo, M
AU  - Iyo M
AD  - Division of Cortical Function Disorders, National Institute of Neuroscience, 
      National Center of Neurology and Psychiatry, Tokyo.Division of Drug Dependence 
      and Psychotropic Drug Clinical Research, National Institute of Mental Health, 
      Chiba, Japan.
LA  - eng
PT  - Journal Article
PL  - United States
TA  - Addict Biol
JT  - Addiction biology
JID - 9604935
EDAT- 1997/07/01 00:00
MHDA- 1997/07/01 00:01
CRDT- 2016/01/07 06:00
PHST- 2016/01/07 06:00 [entrez]
PHST- 1997/07/01 00:00 [pubmed]
PHST- 1997/07/01 00:01 [medline]
AID - 10.1080/13556219772615 [doi]
PST - ppublish
SO  - Addict Biol. 1997 Jul;2(3):317-26. doi: 10.1080/13556219772615.