Risperidone attenuates and reverses hyperthermia induced by 3,4-methylenedioxymethamphetamine (MDMA) in rats

Shioda, Katsutoshi; Nisijima, Koichi; Yoshino, Tatsuki; Kuboshima, Kyoko; Iwamura, Tatsunori; Yui, Kunio; Kato, Satoshi

doi:10.1016/j.neuro.2008.07.005

Cited by 52 publications

(42 citation statements)

References 46 publications

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“…MDMA was shown to cause acute dose-dependent hyperthermia in many laboratory animals, namely, in mice [51,[133][134][135][136][137][138][139][140][141], rats [142][143][144][145][146][147][148][149][150][151][152][153][154][155][156], in rabbits [157,158], guinea pigs [159], and pigs [160]. In unrestrained non-human primates, MDMA was also shown to dose-dependently increase body temperature, leading to hyperthermia [161][162][163][164].…”

Section: Mdma-induced Hyperthermia To Experimental Animalsmentioning

confidence: 99%

Molecular and Cellular Mechanisms of Ecstasy-Induced Neurotoxicity: An Overview

et al. 2009

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"Ecstasy" [(+/-)-3,4-methylenedioxymethamphetamine, MDMA, XTC, X, E] is a psychoactive recreational hallucinogenic substance and a major worldwide drug of abuse. Several reports raised the concern that MDMA has the ability to induce neurotoxic effects both in laboratory animals and humans. Despite more than two decades of research, the mechanisms by which MDMA is neurotoxic are still to be fully elucidated. MDMA induces serotonergic terminal loss in rats and also in some mice strains, but also a broader neuronal degeneration throughout several brain areas such as the cortex, hippocampus, and striatum. Meanwhile, in human "ecstasy" abusers, there are evidences for deficits in seronergic biochemical markers, which correlate with long-term impairments in memory and learning. There are several factors that contribute to MDMA-induced neurotoxicity, namely, hyperthermia, monoamine oxidase metabolism of dopamine and serotonin, dopamine oxidation, the serotonin transporter action, nitric oxide, and the formation of peroxinitrite, glutamate excitotoxicity, serotonin 2A receptor agonism, and, importantly, the formation of MDMA neurotoxic metabolites. The present review covered the following topics: history and epidemiology, pharmacological mechanisms, metabolic pathways and the influence of isoenzyme genetic polymorphisms, as well as the acute effects of MDMA in laboratory animals and humans, with a special focus on MDMA-induced neurotoxic effects at the cellular and molecular level. The main aim of this review was to contribute to the understanding of the cellular and molecular mechanisms involved in MDMA neurotoxicity, which can help in the development of therapeutic approaches to prevent or treat the long-term neuropsychiatric complications of MDMA abuse in humans.

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Section: Mdma-induced Hyperthermia To Experimental Animalsmentioning

confidence: 99%

Molecular and Cellular Mechanisms of Ecstasy-Induced Neurotoxicity: An Overview

et al. 2009

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“…The selective 5-HT 2C antagonist SB-242084 was also dissolved in water for injection and injected at a volume of 3 ml/kg of body weight. The doses of the serotoninergic compounds and cocaine were selected based on findings from the literature employing these drugs in animal behavioral models (Cryan and Lucki 2000;Fox et al 2009;Shioda et al 2008;Vlachou et al 2003Vlachou et al , 2008Zaniewska et al 2009). …”

Section: Drugs and Drug Administrationmentioning

confidence: 99%

Role of serotonin 5-HT2A and 5-HT2C receptors on brain stimulation reward and the reward-facilitating effect of cocaine

2010

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“…Determination of the mechanisms mediating the toxicity associated with co-ingestion of caffeine with MDMA is an important step toward the treatment of severe hyperthermic reactions to ecstasy that occur in some users. Previously Shioda et al (2008) reported that treatment with the atypical antipsychotic drug risperidone attenuates hyperthermia induced by MDMA in rats. Risperidone blocks dopamine D 2 and serotonin 5-HT 2A receptors and other 5-HT receptor types in addition to a weaker blockade on dopamine D 1 receptors.…”

Section: Discussionmentioning

confidence: 99%

“…Sulpiride is a highly selective antagonist commonly used to block central dopamine D 2 receptor-mediated responses in rats at parenteral doses of up to 100 mg/kg (Kaneno et al 2001;O'Tuathaigh and Moran 2004). Shioda et al (2008) have previously reported that, in contrast to SCH 23390 (0.5 mg/kg), pre-treatment with sulpiride (50 mg/kg) does not prevent MDMAinduced hyperthermia.…”

Section: Drug Preparation and Administrationmentioning

confidence: 99%