PMID- 16378215
OWN - NLM
STAT- MEDLINE
DCOM- 20060614
LR  - 20181113
IS  - 0033-3158 (Print)
IS  - 0033-3158 (Linking)
VI  - 184
IP  - 2
DP  - 2006 Jan
TI  - 3,4-Methylenedioxymethamphetamine enhances the release of acetylcholine in the 
      prefrontal cortex and dorsal hippocampus of the rat.
PG  - 182-9
AB  - RATIONALE: The neurochemical effects produced by acute administration of 
      3,4-methylenedioxymethamphetamine (MDMA) on the monoaminergic systems in the 
      brain are well documented; however, there has been little consideration of the 
      potential effects of MDMA on other neurotransmitter systems. OBJECTIVE: The 
      present study was designed to investigate the acute effect of MDMA on cholinergic 
      neurons by measuring acetylcholine (ACh) release in the medial prefrontal cortex 
      (PFC) and dorsal hippocampus, terminal regions of cholinergic projection neurons 
      originating in the basal forebrain. METHODS: In vivo microdialysis and 
      high-performance liquid chromatography with electrochemical detection (HPLC-ED) 
      were used to assess the effects of MDMA on the extracellular concentration of ACh 
      in the PFC and dorsal hippocampus of the rat. RESULTS: The systemic 
      administration of MDMA (3-20 mg/kg, i.p.) resulted in an increased extracellular 
      concentration of ACh in the PFC and dorsal hippocampus. Reverse dialysis of MDMA 
      (100 microM) into the PFC and hippocampus also increased ACh release in these 
      brain regions. Treatment with parachlorophenylalanine and 
      alpha-methyl-para-tyrosine, inhibitors of serotonin (5-HT) and dopamine (DA) 
      synthesis, respectively, significantly attenuated the release of ACh stimulated 
      by MDMA in the PFC, but not in the dorsal hippocampus. CONCLUSIONS: MDMA exerts a 
      stimulatory effect on the release of ACh in the PFC and dorsal hippocampus in 
      vivo, possibly by mechanisms localized within these brain regions. In addition, 
      these results suggest that the MDMA-induced release of ACh in the PFC involves 
      both serotonergic and dopaminergic mechanisms.
FAU - Nair, Sunila G
AU  - Nair SG
AD  - Division of Pharmaceutical Sciences, College of Pharmacy, University of 
      Cincinnati, Cincinnati, OH, 45267, USA.
FAU - Gudelsky, Gary A
AU  - Gudelsky GA
LA  - eng
GR  - DA 07427/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20051224
PL  - Germany
TA  - Psychopharmacology (Berl)
JT  - Psychopharmacology
JID - 7608025
RN  - 0 (Dopamine Uptake Inhibitors)
RN  - 0 (Hallucinogens)
RN  - CK833KGX7E (Amphetamine)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - N9YNS0M02X (Acetylcholine)
SB  - IM
MH  - Acetylcholine/*metabolism
MH  - Amphetamine/pharmacology
MH  - Animals
MH  - Chromatography, High Pressure Liquid
MH  - Dopamine Uptake Inhibitors/pharmacology
MH  - Electrochemistry
MH  - Extracellular Space/drug effects/metabolism
MH  - Hallucinogens/administration & dosage/*pharmacology
MH  - Hippocampus/drug effects/*metabolism
MH  - Male
MH  - Microdialysis
MH  - N-Methyl-3,4-methylenedioxyamphetamine/administration & dosage/*pharmacology
MH  - Prefrontal Cortex/drug effects/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
EDAT- 2005/12/27 09:00
MHDA- 2006/06/15 09:00
CRDT- 2005/12/27 09:00
PHST- 2005/04/25 00:00 [received]
PHST- 2005/11/10 00:00 [accepted]
PHST- 2005/12/27 09:00 [pubmed]
PHST- 2006/06/15 09:00 [medline]
PHST- 2005/12/27 09:00 [entrez]
AID - 10.1007/s00213-005-0271-5 [doi]
PST - ppublish
SO  - Psychopharmacology (Berl). 2006 Jan;184(2):182-9. doi: 10.1007/s00213-005-0271-5. 
      Epub 2005 Dec 24.