PMID- 1358088
OWN - NLM
STAT- MEDLINE
DCOM- 19921221
LR  - 20150311
IS  - 0893-133X (Print)
IS  - 0893-133X (Linking)
VI  - 7
IP  - 2
DP  - 1992 Sep
TI  - Serotonin 5-HT1-like receptors mediate hyperactivity in rats induced by 
      3,4-methylenedioxymethamphetamine.
PG  - 113-27
AB  - This study was designed to evaluate the role of different serotonin (5-HT) 
      receptor subtypes in mediating the effects of 3,4-methylenedioxymethamphetamine 
      (MDMA) on rat exploration of a novel environment. The active enantiomer of MDMA, 
      S-MDMA increases forward locomotion and suppresses investigatory behaviors and 
      local movements. Previous studies indicate that S-MDMA-induced hyperactivity 
      depends upon drug-induced 5-HT release. Propranolol and pindolol, 
      beta-noradrenergic antagonists with affinity for 5-HT1 receptors, antagonized the 
      S-MDMA-induced locomotor hyperactivity. The antagonism by propranolol was 
      stereoselective. In contrast, a beta-noradrenergic antagonist that is a weaker 
      antagonist of 5-HT receptors, betaxolol, was much less effective at blocking the 
      behavioral response to S-MDMA. Among nonselective 5-HT antagonists, methiothepin 
      was effective and methysergide and cyproheptadine were ineffective as antagonists 
      of S-MDMA-induced hypermotility. In other systems, methiothepin has been found to 
      be a good antagonist at 5-HT1B receptors where methysergide and cyproheptadine 
      are ineffective. The 5-HT2 antagonist ritanserin was ineffective in blocking 
      S-MDMA-induced hypermotility. However, ritanserin, methysergide, and 
      cyproheptadine partially reversed the S-MDMA-induced suppression of investigatory 
      responding, suggesting a contribution of 5-HT2 receptor activation to this 
      component of the behavioral response to S-MDMA. This study indicates that S-MDMA 
      produces a characteristic form of locomotor hyperactivity in rats that depends 
      upon activation of 5-HT1-like receptors, possibly of the 5-HT1B subtype.
FAU - Callaway, C W
AU  - Callaway CW
AD  - Department of Psychiatry, University of California, San Diego School of Medicine, 
      La Jolla 92093-0804.
FAU - Rempel, N
AU  - Rempel N
FAU - Peng, R Y
AU  - Peng RY
FAU - Geyer, M A
AU  - Geyer MA
LA  - eng
GR  - DA02925/DA/NIDA NIH HHS/United States
GR  - M07198/PHS HHS/United States
GR  - MH00188/MH/NIMH NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Neuropsychopharmacology
JT  - Neuropsychopharmacology : official publication of the American College of 
      Neuropsychopharmacology
JID - 8904907
RN  - 0 (Adrenergic beta-Antagonists)
RN  - 0 (Receptors, Serotonin)
RN  - 0 (Serotonin Antagonists)
RN  - 4764-17-4 (3,4-Methylenedioxyamphetamine)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
SB  - IM
MH  - 3,4-Methylenedioxyamphetamine/*analogs & derivatives/antagonists & 
      inhibitors/pharmacology
MH  - Adrenergic beta-Antagonists/pharmacology
MH  - Animals
MH  - Behavior, Animal/drug effects
MH  - Male
MH  - Motor Activity/*drug effects
MH  - N-Methyl-3,4-methylenedioxyamphetamine
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Serotonin/*drug effects
MH  - Serotonin Antagonists/pharmacology
EDAT- 1992/09/01 00:00
MHDA- 1992/09/01 00:01
CRDT- 1992/09/01 00:00
PHST- 1992/09/01 00:00 [pubmed]
PHST- 1992/09/01 00:01 [medline]
PHST- 1992/09/01 00:00 [entrez]
PST - ppublish
SO  - Neuropsychopharmacology. 1992 Sep;7(2):113-27.