Abstract
Methamphetamine (METH) and its derivative 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) are 2 substituted amphetamines with very high abuse liability in the United States. These amphetamine-like stimulants have been associated with loss of multiple markers for dopaminergic and serotonergic terminals in the brain. Among other causes, oxidative stress, excitotoxicity and mitochondrial dysfunction appear to play a major role in the neurotoxicity produced by the substituted amphetamines. The present review will focus on these events and how they interact and converge to produce the monoaminergic depletions that are typically observed after METH or MDMA administration. In addition, more recently identified consequences of METH or MDMA-induced oxidative stress, excitotoxicity, and mitochondrial dysfunction are described in relation to the classical markers of METH-induced damage to dopamine terminals.
| Original language | English (US) |
|---|---|
| Article number | 38 |
| Pages (from-to) | E337-E347 |
| Journal | AAPS Journal |
| Volume | 8 |
| Issue number | 2 |
| DOIs | |
| State | Published - May 12 2006 |
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Keywords
- Blood-brain barrier
- Excitotoxicity
- Glutamate
- Mitochondrial dysfunction
- Oxidative stress
- Substituted amphetamines
ASJC Scopus subject areas
- Pharmaceutical Science
Cite this
Causes and consequences of methamphetamine and MDMA toxicity. / Quinton, Maria S.; Yamamoto, Bryan K.
In: AAPS Journal, Vol. 8, No. 2, 38, 12.05.2006, p. E337-E347.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Causes and consequences of methamphetamine and MDMA toxicity
AU - Quinton, Maria S.
AU - Yamamoto, Bryan K.
PY - 2006/5/12
Y1 - 2006/5/12
N2 - Methamphetamine (METH) and its derivative 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) are 2 substituted amphetamines with very high abuse liability in the United States. These amphetamine-like stimulants have been associated with loss of multiple markers for dopaminergic and serotonergic terminals in the brain. Among other causes, oxidative stress, excitotoxicity and mitochondrial dysfunction appear to play a major role in the neurotoxicity produced by the substituted amphetamines. The present review will focus on these events and how they interact and converge to produce the monoaminergic depletions that are typically observed after METH or MDMA administration. In addition, more recently identified consequences of METH or MDMA-induced oxidative stress, excitotoxicity, and mitochondrial dysfunction are described in relation to the classical markers of METH-induced damage to dopamine terminals.
AB - Methamphetamine (METH) and its derivative 3,4-methylenedioxymethamphetamine (MDMA; ecstasy) are 2 substituted amphetamines with very high abuse liability in the United States. These amphetamine-like stimulants have been associated with loss of multiple markers for dopaminergic and serotonergic terminals in the brain. Among other causes, oxidative stress, excitotoxicity and mitochondrial dysfunction appear to play a major role in the neurotoxicity produced by the substituted amphetamines. The present review will focus on these events and how they interact and converge to produce the monoaminergic depletions that are typically observed after METH or MDMA administration. In addition, more recently identified consequences of METH or MDMA-induced oxidative stress, excitotoxicity, and mitochondrial dysfunction are described in relation to the classical markers of METH-induced damage to dopamine terminals.
KW - Blood-brain barrier
KW - Excitotoxicity
KW - Glutamate
KW - Mitochondrial dysfunction
KW - Oxidative stress
KW - Substituted amphetamines
UR - http://www.scopus.com/inward/record.url?scp=33646920890&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=33646920890&partnerID=8YFLogxK
U2 - 10.1208/aapsj080238
DO - 10.1208/aapsj080238
M3 - Review article
C2 - 16796384
AN - SCOPUS:33646920890
VL - 8
SP - E337-E347
JO - AAPS Journal
JF - AAPS Journal
SN - 1550-7416
IS - 2
M1 - 38
ER -