MDMA (3,4-methylenedioxymethamphetamine) or ecstasy: the contemporary human and animal research perspective

Parrott, Andrew C.; Marsden, C.A.

doi:10.1177/0269881106063263

Cited by 10 publications

(6 citation statements)

References 36 publications

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“…The behavioural changes occurring as a result of MDMA pre‐exposure are not only social in nature: pre‐exposed rats show prolonged increases in anxiety on the elevated plus maze and emergence tests, have poorer memory than controls and are impaired in their coping responses to acute stress in the forced swim test ( Morley et al ., 2001 ; McGregor et al ., 2003b ; Thompson et al ., 2004 ). These effects are mirrored in some recent studies of human MDMA users, where anxiety and depressive disorders may be over‐represented and impairment in processing of social cues is evident ( Parrott and Marsden, 2006 ; Reay et al ., 2006 ).…”

Section: Residual Social Deficits Caused By Drug Exposurementioning

confidence: 70%

From ultrasocial to antisocial: a role for oxytocin in the acute reinforcing effects and long‐term adverse consequences of drug use?

McGregor¹,

Callaghan²,

Hunt³

2008

British J Pharmacology

160

114

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Addictive drugs can profoundly affect social behaviour both acutely and in the long-term. Effects range from the artificial sociability imbued by various intoxicating agents to the depressed and socially withdrawn state frequently observed in chronic drug users. Understanding such effects is of great potential significance in addiction neurobiology. In this review we focus on the 'social neuropeptide' oxytocin and its possible role in acute and long-term effects of commonly used drugs. Oxytocin regulates social affiliation and social recognition in many species and modulates anxiety, mood and aggression. Recent evidence suggests that popular party drugs such as MDMA and gamma-hydroxybutyrate (GHB) may preferentially activate brain oxytocin systems to produce their characteristic prosocial and prosexual effects. Oxytocin interacts with the mesolimbic dopamine system to facilitate sexual and social behaviour, and this oxytocin-dopamine interaction may also influence the acquisition and expression of drug-seeking behaviour. An increasing body of evidence from animal models suggests that even brief exposure to drugs such as MDMA, cannabinoids, methamphetamine and phencyclidine can cause long lasting deficits in social behaviour. We discuss preliminary evidence that these adverse effects may reflect long-term neuroadaptations in brain oxytocin systems. Laboratory studies and preliminary clinical studies also indicate that raising brain oxytocin levels may ameliorate acute drug withdrawal symptoms. It is concluded that oxytocin may play an important, yet largely unexplored, role in drug addiction. Greater understanding of this role may ultimately lead to novel therapeutics for addiction that can improve mood and facilitate the recovery of persons with drug use disorders.

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Section: Residual Social Deficits Caused By Drug Exposurementioning

confidence: 70%

From ultrasocial to antisocial: a role for oxytocin in the acute reinforcing effects and long‐term adverse consequences of drug use?

McGregor¹,

Callaghan²,

Hunt³

2008

British J Pharmacology

160

114

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“…Although in recent years, the question of 'ecstasy'induced neurotoxicity and possible functional sequelae has been addressed in several studies, the extent to which these animal and non-human primate data are applicable to humans and whether persistent neurotoxicity occurs in humans is still controversial [42,[207][208][209][213][214][215][216][217][218][219]. To date, the most consistent findings associate subtle cognitive, particularly memory, impairments with heavy ecstasy abuse [213,218,219].…”

Section: Alterations Of Neurotransmitters and Receptorsmentioning

confidence: 99%

Review: The neuropathology of drug abuse

Büttner

2011

Neuropathology and Applied Neurobiology

151

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Drug abuse represents a significant health issue. The major substances abused include cannabis, opiates, cocaine, amphetamine, methamphetamine and 'ecstasy'. Alterations of intracellular messenger pathways, transcription factors and immediate early genes within the brain reward system seem to be fundamentally important for the development of addiction and chronic drug abuse. Genetic risk factors and changes in gene expression associated with drug abuse are still poorly understood. Besides cardiovascular complications, psychiatric and neurologic symptoms are the most common manifestations of drug toxicity. A broad spectrum of changes affecting the central nervous system is seen in drug abusers. The major findings result from the consequences of ischaemia and cerebrovascular diseases. Except for a few observations of vasculitis, the aetiology of these cerebrovascular accidents is not fully understood. The abuse of amphetamine, methamphetamine and MDMA has been related to neurotoxicity in human long-term abusers and to the risk of developing Parkinson's disease. However, whether such neurotoxicity occurs remain to be established. Systematic histological, immunohistochemical and morphometric investigations have shown profound morphological alterations in the brains of polydrug abusers. The major findings comprise neuronal loss, neurodegenerative alterations, a reduction of glial fibrillary acidic protein-immunopositive astrocytes, widespread axonal damage with concomitant microglial activation as well as reactive and degenerative changes of the cerebral microvasculature. These observations demonstrate that drugs of abuse initiate a cascade of interacting toxic, vascular and hypoxic factors, which finally result in widespread disturbances within the complex network of central nervous system cell-to-cell interactions.

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“…Studying the problem is difficult because different experimental animals respond differently both from other models and from humans [11,17]. In general, the acute effects of MDMA seem to be more or less the same in most animal models, but the models diverge widely when it comes to their ability to produce the changes induced by chronic exposure [27]. Clearly, our study has demonstrated that cellular injury has occurred, but by the very nature of our experimental design, we are unable to assess many of the other issues that we know exist as hyperthermia, dehydration and rhabdomyolysis.…”

Section: Discussionmentioning

confidence: 99%

Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (MDMA) administration in a rat model

et al. 2008

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Experimental and clinical data indicate that 3,4-methylenedioxy-N-methylamphetamine (MDMA) abuse can produce significant cardiovascular toxicity. A mechanism may be a direct toxic effect of redox active metabolites of MDMA. To evaluate the effect of a single MDMA dose on cellular antioxidant defence system and to investigate the morphology in male albino rats, total glutathione (GSH), oxidised glutathione (GSSG), ascorbic acid (AA), glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD) and malondialdehyde (MDAL) were studied. The effects were evaluated at 3, 6, 16 and 24 h after MDMA administration. Antioxidant enzymes activity was significantly reduced: GPx (-24%) and SOD (-50%) after 3 h and GR (-19%) after 6 h from treatment. AA levels decrease (-37%) after 3 h and (-30%) after 6 h; MDAL level increased (+119%) after 3 h; GSH levels decreased after 3 (31.3%) and 6 h (37.9%) from MDMA treatment. GSSG content was not affected by ecstasy administration. Myocardial contraction band necrosis (CBN) was already visible in rats killed at 6 h. After 16 h, macrophagic monocytes around the necrotic myocardial cells were observed, and within 24 h, this infiltrate became more widespread with an early removal of the necrotic material. Calcium deposits were observed within ventricular cardiomyocytes with intact nuclei and sarcomeres. Single administration of MDMA can significantly alter the cellular antioxidant defence system and produce oxidative stress which may result in lipid peroxidation and disruption of Ca(2 +) homeostasis. The depression in Ca(2+) regulatory mechanism by reactive oxygen species ultimately results in intracellular Ca(2 +) overload, CBN and cell death.

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MDMA (3,4-methylenedioxymethamphetamine) or ecstasy: the contemporary human and animal research perspective

Cited by 10 publications

References 36 publications

From ultrasocial to antisocial: a role for oxytocin in the acute reinforcing effects and long‐term adverse consequences of drug use?

From ultrasocial to antisocial: a role for oxytocin in the acute reinforcing effects and long‐term adverse consequences of drug use?

Review: The neuropathology of drug abuse

Cardiac oxidative stress determination and myocardial morphology after a single ecstasy (MDMA) administration in a rat model

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