Causes and consequences of methamphetamine and MDMA toxicity

Quinton, Maria S.; Yamamoto, Bryan K.

doi:10.1007/bf02854904

Cited by 126 publications

(92 citation statements)

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%

“…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%

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Behavioral sensitization and cross-sensitization between methylphenidate amphetamine, and 3,4-methylenedioxymethamphetamine (MDMA) in female SD rats

Peng

Atkins²,

Dafny³

2011

European Journal of Pharmacology

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The psychostimulants amphetamine and methylphenidate (MPD / Ritalin) are the drugs most often used to treat attention deficit hyperactivity disorder (ADHD). In addition, students of all ages take these drugs to improve academic performance but also abuse them for pleasurable enhancement. In addition, other psychostimulants such 3,4 methylenedioxymethamphetamine (MDMA / ecstasy) are used / abused for similar objectives. One of the experimental markers for the potential of a drug to produce dependence is its ability to induce behavioral sensitization and cross sensitization with other drugs of abuse. The objective of this study is to use identical experimental protocols and behavioral assays to compare in female rats the effects of amphetamine, MPD and MDMA on locomotor activity and to determine if they induce behavioral sensitization and/or cross sensitization with each other. The main findings of this study are 1. Acute amphetamine, MPD and MDMA all elicited increases in locomotor activity. 2. Chronic administration of an intermediate dose of amphetamine or MPD elicited behavioral sensitization. 3. Chronic administration of MDMA elicited behavioral sensitization in some animals and behavioral tolerance in others. 4. Cross sensitization between MPD and amphetamine was observed. 5. MDMA did not show either cross sensitization or cross tolerance with amphetamine. In conclusion, these results suggest that MDMA act by different mechanisms compared to MPD and amphetamine.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Behavioral sensitization and cross-sensitization between methylphenidate amphetamine, and 3,4-methylenedioxymethamphetamine (MDMA) in female SD rats

Peng

Atkins²,

Dafny³

2011

European Journal of Pharmacology

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“…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%

Neurochemical Alterations in Methamphetamine-Dependent Patients Treated with Cytidine-5′-Diphosphate Choline: A Longitudinal Proton Magnetic Resonance Spectroscopy Study

Yoon

Lyoo

Kim

et al. 2009

Neuropsychopharmacol

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Cytidine-5 0 -diphosphate choline (CDP-choline), as an important intermediate for major membrane phospholipids, may exert neuroprotective effects in various neurodegenerative disorders. This longitudinal proton magnetic resonance spectroscopy ( 1 H-MRS) study aimed to examine whether a 4-week CDP-choline treatment could alter neurometabolite levels in patients with methamphetamine (MA) dependence and to investigate whether changes in neurometabolite levels would be associated with MA use. We hypothesized that the prefrontal levels of N-acetyl-aspartate (NAA), a neuronal marker, and choline-containing compound (Cho), which are related to membrane turnover, would increase with CDP-choline treatment in MA-dependent patients. We further hypothesized that this increase would correlate with the total number of negative urine results. Thirty-one treatment seekers with MA dependence were randomly assigned to receive CDP-choline (n ¼ 16) or placebo (n ¼ 15) for 4 weeks. Prefrontal NAA and Cho levels were examined using 1 H-MRS before medication, and at 2 and 4 weeks after treatment. Generalized estimating equation regression analyses showed that the rate of change in prefrontal NAA (p ¼ 0.005) and Cho (p ¼ 0.03) levels were greater with CDP-choline treatment than with placebo. In the CDP-choline-treated patients, changes in prefrontal NAA levels were positively associated with the total number of negative urine results (p ¼ 0.03). Changes in the prefrontal Cho levels, however, were not associated with the total number of negative urine results. These preliminary findings suggest that CDP-choline treatment may exert potential neuroprotective effects directly or indirectly because of reductions in drug use by the MA-dependent patients. Further studies with a larger sample size of MA-dependent patients are warranted to confirm a long-term efficacy of CDP-choline in neuroprotection and abstinence.

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“…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%

Glial Modulators as Potential Treatments of Psychostimulant Abuse

Beardsley

Hauser

2014

Advances in Pharmacology

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Glia (including astrocytes, microglia and oligodendrocytes), which constitute the majority of cells in the brain. have many of the same receptors as neurons, secrete neurotransmitters and neurotrophic and neuroinflammatory factors, control clearance of neurotransmitters from synaptic clefts, and are intimately involved in synaptic plasticity. Despite their prevalence and spectrum of functions, appreciation of their potential general importance has been elusive since their identification in the mid-1800s, and only relatively recently have they been gaining their due respect. This development of appreciation has been nurtured by the growing awareness that drugs of abuse, including the psychostimulants, affect glial activity, and glial activity, in turn, has been found to modulate the effects of the psychostimulants. This developing awareness has begun to illuminate novel pharmacotherapeutic targets for treating psychostimulant abuse, for which targeting more conventional neuronal targets has not yet resulted in a single, approved medication. In this chapter, we discuss the molecular pharmacology, physiology and functional relationships that the glia have especially in the light in which they present themselves as targets for pharmacotherapeutics intended to treat psychostimulant abuse disorders. We then review a cross section of preclinical studies that have manipulated glial processes whose behavioral effects have been supportive of considering the glia as drug targets for psychostimulant-abuse medications. We then close with comments regarding the current clinical evaluation of relevant compounds for treating psychostimulant abuse, as well as the likelihood of future prospects.

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Causes and consequences of methamphetamine and MDMA toxicity

Cited by 126 publications

References 79 publications

Behavioral sensitization and cross-sensitization between methylphenidate amphetamine, and 3,4-methylenedioxymethamphetamine (MDMA) in female SD rats

Behavioral sensitization and cross-sensitization between methylphenidate amphetamine, and 3,4-methylenedioxymethamphetamine (MDMA) in female SD rats

Neurochemical Alterations in Methamphetamine-Dependent Patients Treated with Cytidine-5′-Diphosphate Choline: A Longitudinal Proton Magnetic Resonance Spectroscopy Study

Glial Modulators as Potential Treatments of Psychostimulant Abuse

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