PMID- 9506825
OWN - NLM
STAT- MEDLINE
DCOM- 19980511
LR  - 20190921
IS  - 0162-3109 (Print)
IS  - 0162-3109 (Linking)
VI  - 38
IP  - 3
DP  - 1998 Jan
TI  - Acute 3,4-methylenedioxymethamphetamine(MDMA) administration produces a rapid and 
      sustained suppression of immune function in the rat.
PG  - 253-60
AB  - (+)-3,4-Methylenedioxymethamphetamine (MDMA;'Ecstasy') is a ring substituted 
      phenylisopropylamine that is structurally related to both amphetamines and 
      hallucinogens. The unique behavioural activating properties of MDMA have led to 
      its widespread abuse. MDMA induces many neurochemical, behavioural and endocrine 
      alterations which closely resemble those elicited by exposure to acute stress, 
      suggesting that MDMA could be regarded as a 'chemical stressor'. In addition to 
      the neurochemical, behavioural and endocrine effects of stressor exposure, it has 
      been reported that stress produces alterations in immune function. However, to 
      date the effects of MDMA on immune function have been restricted to in vitro 
      investigations. In this study we report, for the first time, that acute in vivo 
      administration of MDMA (20 mg/kg, i.p.) produced a rapid (within 30 min) 
      suppression of Con A-induced lymphocyte proliferation and a profound reduction in 
      the total leucocyte count in rats that persisted for at least 6 h following 
      injection. These alterations in immune function were accompanied by a significant 
      increase in plasma corticosterone concentrations 30 min post MDMA administration 
      which had returned to baseline values within 6 h of drug administration. In 
      addition, there was a significant depletion in cortical 5-HT concentrations both 
      30 min and 6 h after MDMA administration. The results of this study provide 
      evidence that in addition to the well established toxic effects of MDMA on the 
      central serotonergic system, a single administration of this widely abused drug 
      induces a rapid and sustained suppression of immune function.
FAU - Connor, T J
AU  - Connor TJ
AD  - Department of Pharmacology, University College Galway, Ireland.
FAU - McNamara, M G
AU  - McNamara MG
FAU - Finn, D
AU  - Finn D
FAU - Currid, A
AU  - Currid A
FAU - O'Malley, M
AU  - O'Malley M
FAU - Redmond, A M
AU  - Redmond AM
FAU - Kelly, J P
AU  - Kelly JP
FAU - Leonard, B E
AU  - Leonard BE
LA  - eng
PT  - Journal Article
PL  - Netherlands
TA  - Immunopharmacology
JT  - Immunopharmacology
JID - 7902474
RN  - 0 (Hallucinogens)
RN  - 0 (Serotonin Agents)
RN  - 11028-71-0 (Concanavalin A)
RN  - 333DO1RDJY (Serotonin)
RN  - 54-16-0 (Hydroxyindoleacetic Acid)
RN  - KE1SEN21RM (N-Methyl-3,4-methylenedioxyamphetamine)
RN  - W980KJ009P (Corticosterone)
SB  - IM
MH  - Animals
MH  - Cerebral Cortex/drug effects/metabolism
MH  - Concanavalin A
MH  - Corticosterone/blood
MH  - Female
MH  - Hallucinogens/administration & dosage/*toxicity
MH  - Hydroxyindoleacetic Acid/analysis/metabolism
MH  - Immunity, Cellular/*drug effects
MH  - Leukocyte Count/drug effects
MH  - Lymphocyte Activation/drug effects
MH  - N-Methyl-3,4-methylenedioxyamphetamine/administration & dosage/*toxicity
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Serotonin/analysis/metabolism
MH  - Serotonin Agents/administration & dosage/*toxicity
MH  - T-Lymphocytes/*drug effects/immunology
MH  - Time Factors
EDAT- 1998/03/20 00:00
MHDA- 1998/03/20 00:01
CRDT- 1998/03/20 00:00
PHST- 1998/03/20 00:00 [pubmed]
PHST- 1998/03/20 00:01 [medline]
PHST- 1998/03/20 00:00 [entrez]
AID - S0162310997000842 [pii]
AID - 10.1016/s0162-3109(97)00084-2 [doi]
PST - ppublish
SO  - Immunopharmacology. 1998 Jan;38(3):253-60. doi: 10.1016/s0162-3109(97)00084-2.