PMID- 11888574
OWN - NLM
STAT- MEDLINE
DCOM- 20020911
LR  - 20190712
IS  - 0091-3057 (Print)
IS  - 0091-3057 (Linking)
VI  - 71
IP  - 4
DP  - 2002 Apr
TI  - Recreational Ecstasy/MDMA, the serotonin syndrome, and serotonergic 
      neurotoxicity.
PG  - 837-44
AB  - The ring-substituted amphetamine derivative 3,4-methylenedioxymethamphetamine 
      (MDMA) or "Ecstasy" is widely used a recreational drug. It stimulates the release 
      and inhibits the reuptake of serotonin (5-HT) and other neurotransmitters such as 
      dopamine to a lesser extent. The acute boost in monoamine activity can generate 
      feelings of elation, emotional closeness, and sensory pleasure. In the hot and 
      crowded conditions of raves/dances, mild versions of the serotonin syndrome often 
      develop, when hyperthermia, mental confusion, and hyperkinesia predominate. Rest 
      in a cooler environment generally reverses these problems, although they can 
      develop into medical emergencies, which occasionally prove fatal. This acute 
      serotonergic overactivity is exacerbated by the high ambient temperatures, 
      overcrowding (aggregate toxicity), and use of other stimulant drugs. The on-drug 
      experience is generally followed by negative moods, with 80--90% of weekend 
      Ecstasy users reporting 'midweek blues', due probably to monoaminergic depletion. 
      Single doses of MDMA can cause serotonergic nerve damage in laboratory animals, 
      with repeated doses causing extensive loss of distal axon terminals. Huether's 
      explanatory model for this 5-HT neurotoxicity will be briefly described. There is 
      an increasing body of evidence for equivalent neuropsychobiological damage in 
      humans. Abstinent regular Ecstasy users often show: reduced cerebrospinal 5-HIAA, 
      reduced density of 5-HT transporters, blunted response to a fenfluramine 
      challenge, memory problems, higher cognitive deficits, various psychiatric 
      disorders, altered appetite, and loss of sexual interest. Functional deficits may 
      remain long after drug use has ceased and are consistent with serotonergic axonal 
      loss in higher brain regions.
FAU - Parrott, A C
AU  - Parrott AC
AD  - Department of Psychology, University of East London, E15 4LZ, London, UK. 
      a.c.parrott@uel.ac.uk
LA  - eng
PT  - Journal Article
PT  - Review
PL  - United States
TA  - Pharmacol Biochem Behav
JT  - Pharmacology, biochemistry, and behavior
JID - 0367050
RN  - 0 (Serotonin Agents)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - Animals
MH  - Cognition Disorders/chemically induced/psychology
MH  - Humans
MH  - Memory Disorders/chemically induced/psychology
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*adverse effects/toxicity
MH  - Neurotoxicity Syndromes/*physiopathology
MH  - Serotonin Agents/*adverse effects/toxicity
MH  - Serotonin Syndrome/*physiopathology
RF  - 68
EDAT- 2002/03/13 10:00
MHDA- 2002/09/12 10:01
CRDT- 2002/03/13 10:00
PHST- 2002/03/13 10:00 [pubmed]
PHST- 2002/09/12 10:01 [medline]
PHST- 2002/03/13 10:00 [entrez]
AID - S0091305701007110 [pii]
AID - 10.1016/s0091-3057(01)00711-0 [doi]
PST - ppublish
SO  - Pharmacol Biochem Behav. 2002 Apr;71(4):837-44. doi: 
      10.1016/s0091-3057(01)00711-0.