PMID- 11842446
OWN - NLM
STAT- MEDLINE
DCOM- 20020503
LR  - 20181130
IS  - 0887-4476 (Print)
IS  - 0887-4476 (Linking)
VI  - 44
IP  - 1
DP  - 2002 Apr
TI  - Altered prolactin response to M-chlorophenylpiperazine in monkeys previously 
      treated with 3,4-methylenedioxymethamphetamine (MDMA) or fenfluramine.
PG  - 51-7
AB  - 3,4-Methylenedioxymethamphetamine ("Ecstasy," MDMA) and fenfluramine, widely used 
      by humans, are potent brain serotonin (5-HT) neurotoxins in animals. Thus, there 
      is concern that humans previously exposed to these amphetamine derivatives may 
      have incurred brain 5-HT neurotoxicity. However, assessing the status of brain 
      5-HT neurons in the living organism is challenging. To determine whether MDMA- 
      and/or fenfluramine-induced 5-HT neurotoxicity can be detected during life using 
      neuroendocrine methods, groups of monkeys previously treated with neurotoxic 
      regimens of MDMA or fenfluramine, along with saline-treated controls, underwent 
      neuroendocrine challenge with the direct 5-HT agonist and 5-HT-releasing drug, 
      m-chlorophenylpiperazine (m-CPP). Animals treated 2 weeks previously with MDMA 
      exhibited a nonsignificant reduction in the prolactin response to m-CPP. In 
      contrast, monkeys treated 3 1/2 years previously with MDMA or 2 years previously 
      with fenfluramine exhibited significantly increased prolactin responses to m-CPP. 
      No significant differences in cortisol concentrations were noted between groups 
      at any time point. These data indicate that neuroendocrine challenge with m-CPP 
      is capable of detecting substituted amphetamine-induced 5-HT neurotoxicity in 
      living primates, but that the recency of drug exposure is an important 
      consideration. Changes in the neuroendocrine response to m-CPP over time in 
      animals with substituted amphetamine-induced neurotoxicity may be related to 
      aberrant 5-HT reinnervation of the basal forebrain that occurs over time in 
      monkeys previously treated with neurotoxic doses of MDMA or fenfluramine.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Hatzidimitriou, George
AU  - Hatzidimitriou G
AD  - Department of Neurology, The Johns Hopkins School of Medicine, Baltimore, 
      Maryland, USA.
FAU - Tsai, Elizabeth H
AU  - Tsai EH
FAU - McCann, Una D
AU  - McCann UD
FAU - Ricaurte, George A
AU  - Ricaurte GA
LA  - eng
GR  - DA05707/DA/NIDA NIH HHS/United States
GR  - DA05938/DA/NIDA NIH HHS/United States
GR  - DA09487/DA/NIDA NIH HHS/United States
GR  - DA10217/DA/NIDA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Synapse
JT  - Synapse (New York, N.Y.)
JID - 8806914
RN  - 0 (Neurotoxins)
RN  - 0 (Piperazines)
RN  - 0 (Serotonin Agents)
RN  - 2DS058H2CF (Fenfluramine)
RN  - 9002-62-4 (Prolactin)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - REY0CNO998 (1-(3-chlorophenyl)piperazine)
RN  - WI4X0X7BPJ (Hydrocortisone)
SB  - IM
MH  - Animals
MH  - Drug Administration Schedule
MH  - Drug Interactions
MH  - Fenfluramine/*toxicity
MH  - Hydrocortisone/blood/metabolism
MH  - Hypothalamus/drug effects/metabolism
MH  - Male
MH  - N-Methyl-3,4-methylenedioxyamphetamine/*toxicity
MH  - Neurotoxins/*toxicity
MH  - Piperazines/*pharmacology
MH  - Presynaptic Terminals/*drug effects/pathology
MH  - Prolactin/blood/*metabolism
MH  - Raphe Nuclei/*drug effects/pathology/physiopathology
MH  - Reaction Time/drug effects/physiology
MH  - Saimiri
MH  - Serotonin Agents/*toxicity
EDAT- 2002/02/14 10:00
MHDA- 2002/05/04 10:01
CRDT- 2002/02/14 10:00
PHST- 2002/02/14 10:00 [pubmed]
PHST- 2002/05/04 10:01 [medline]
PHST- 2002/02/14 10:00 [entrez]
AID - 10.1002/syn.10055 [pii]
AID - 10.1002/syn.10055 [doi]
PST - ppublish
SO  - Synapse. 2002 Apr;44(1):51-7. doi: 10.1002/syn.10055.