2006
DOI: 10.1007/bf02854904
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Causes and consequences of methamphetamine and MDMA toxicity

Abstract: A BSTRACTMethamphetamine (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 r… Show more

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Cited by 127 publications
(92 citation statements)
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References 79 publications
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“…Dopamine causes the 5-HT axon terminal to become shriveled up and damaged. It takes up to two weeks to replenish serotonin levels after the initial MDMA doses and even longer after larger doses (Quinton and Yamamoto, 2006). The chronic effects of MDMA can cause substantial loss of serotonin reuptake transporters (Quinton and Yamamoto.…”
Section: Discussionmentioning
confidence: 99%
See 1 more Smart Citation
“…Dopamine causes the 5-HT axon terminal to become shriveled up and damaged. It takes up to two weeks to replenish serotonin levels after the initial MDMA doses and even longer after larger doses (Quinton and Yamamoto, 2006). The chronic effects of MDMA can cause substantial loss of serotonin reuptake transporters (Quinton and Yamamoto.…”
Section: Discussionmentioning
confidence: 99%
“…The chronic effects of MDMA can cause substantial loss of serotonin reuptake transporters (Quinton and Yamamoto. 2006) causing irreversible degeneration of serotonin nerve terminals (Quinton and Yamamoto, 2006). Chronic MDMA administration regulates transcription of c-fos and egr-1 genes (Shirayama et al, 2000 and Stephenson et al, 1999) which play a role in converting acute neural stimulation into chronic cellular changes in Neuroplasticity (Herrera and Robertson, 1996 and Thiriet et al, 2002).…”
Section: Discussionmentioning
confidence: 99%
“…Mitochondrial dysfunction has been proposed as one of the important mechanisms for MA neurotoxicity (Davidson et al , 2001; Tian et al , 2009; Quinton and Yamamoto, 2006; Brown and Yamamoto, 2003). Given that NAA is mainly synthesized in mitochondria (Patel and Clark, 1979; Truckenmiller et al , 1985) and that synthesis of NAA requires an energy-dependent step (Patel and Clark, 1979), lower NAA levels have been, in part, considered as a putative marker for mitochondrial dysfunction (Clark, 1998).…”
Section: Discussionmentioning
confidence: 99%
“…Disrupting DC-SIGN alters basic immune function and the ability of dendritic cells to present antigens to T-lymphocytes. Numerous reviews describe the mechanisms by which psychostimulants cause aberrant intracellular redox potentials (Rubartelli & Lotze, 2007), oxidative and nitrosative stress, hyperthermia (Thomas, Walker, Benjamins, Geddes, & Kuhn, 2004), mitochondrial energetics, and glucose metabolism in neurons and glia (Davidson, Gow, Lee, & Ellinwood, 2001; Quinton & Yamamoto, 2006; Krasnova & Cadet, 2009; Cadet & Krasnova, 2009; Kita, Miyazaki, Asanuma, Takeshima, & Wagner, 2009; Kaushal & Matsumoto, 2011; Coller & Hutchinson, 2012; Cadet & Jayanthi, 2013). …”
Section: Molecular Biology and Physiology Of The Gliamentioning
confidence: 99%
“…Methamphetamine and other psychostimulants induce atypical increases in extracellular glutamate in the CNS (Miyatake, Narita, Shibasaki, Nakamura, & Suzuki, 2005; Quinton & Yamamoto, 2006; Cadet, Krasnova, Jayanthi, & Lyles, 2007; Kaushal & Matsumoto, 2011; Pereira et al, 2012). Excessive glutamate, especially at extrasynaptic sites (Sattler, Xiong, Lu, MacDonald, & Tymianski, 2000; Hardingham, Fukunaga, & Bading, 2002), induces excitotoxic injury through actions at specific glutamate receptor types and subtypes expressed by neurons (Rothman & Olney, 1986; Choi, 1988; Olney et al, 1991; Choi, 1992).…”
Section: Molecular Biology and Physiology Of The Gliamentioning
confidence: 99%