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The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”)
TLDR
Evidence for the occurrence of MDMA-induced neurotoxic damage in human users remains equivocal, although some biochemical and functional data suggest that damage may occur in the brains of heavy users.
The relationship between the degree of neurodegeneration of rat brain 5-HT nerve terminals and the dose and frequency of administration of MDMA (`ecstasy')
TLDR
The data demonstrate that MDMA-induced neurodegeneration is related to both the dose and frequency of administration and indicate that damage to 5-HT neurones can occur in the absence of a hyperthermic response to the drug.
The pharmacology of the acute hyperthermic response that follows administration of 3,4‐methylenedioxymethamphetamine (MDMA, ‘ecstasy’) to rats
TLDR
It is suggested that ecstasy‐induced hyperthermia results not from MDMA‐induced 5‐HT release, but rather from the increased release of dopamine that acts at D1 receptors, and has implications for the clinical treatment of MDMA‐ inducedhyperthermia.
3,4-Methylenedioxymethamphetamine induces monoamine release, but not toxicity, when administered centrally at a concentration occurring following a peripherally injected neurotoxic dose
TLDR
It is demonstrated that MDMA when injected directly into the brain produces 5-HT release but no neurotoxicity, suggesting that it must be metabolised peripherally in order to produce compounds that induce free radical formation and neurotoxicity in the brain.
Acute and long-term effects of MDMA on cerebral dopamine biochemistry and function
TLDR
It is suggested more focus be made on the actions of MDMA on dopamine neurochemistry and function to provide a better understanding of the acute and long-term consequences of using this popular recreational drug.
In vivo evidence for free radical involvement in the degeneration of rat brain 5‐HT following administration of MDMA (‘ecstasy’) and p‐chloroamphetamine but not the degeneration following fenfluramine
TLDR
Data indicate that a major mechanism by which MDMA and PCA induce damage to 5‐hydroxytryptaminergic neurones in rat brain is by increasing the formation of free radicals, and suggests that these different modes of action render untenable the recent suggestion that MDMA will not be neurotoxic in humans.
A review of the mechanisms involved in the acute MDMA (ecstasy)-induced hyperthermic response.
TLDR
It is suggested that any MDMA-induced hyperthermic response will be enhanced in hot, crowded dance club conditions and that ingesting the drug in such conditions increases the possibility of subsequent cerebral neurotoxic effect.
The hyperthermic and neurotoxic effects of ‘Ecstasy’ (MDMA) and 3,4 methylenedioxyamphetamine (MDA) in the Dark Agouti (DA) rat, a model of the CYP2D6 poor metabolizer phenotype
TLDR
These data demonstrate that female DA rats are more susceptible to the acute hyperthermic effects of MDMA, probably because of impaired N‐demethylation and indicate that in human subjects acute MDMA‐induced toxicity may be exacerbated in poor metabolizer phenotypes.
Persistent MDMA‐induced dopaminergic neurotoxicity in the striatum and substantia nigra of mice
TLDR
These data provide the first evidence that MDMA causes persistent loss of dopaminergic cell bodies in the SN, as well as a dose‐dependent long‐lasting decrease in TH‐ and DA transporter‐immunoreactivity in the striatum.
A study of the mechanisms involved in the neurotoxic action of 3,4‐methylenedioxymethamphetamine (MDMA, ‘ecstasy’) on dopamine neurones in mouse brain
TLDR
MDMA‐induced neurotoxicity results from MDMA or dopamine metabolites producing radicals that combine with NO to form tissue‐damaging peroxynitrites, and was found to have no radical trapping activity.
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