Ecstasy-induced cell death in cortical neuronal cultures is serotonin 2A-receptor-dependent and potentiated under hyperthermia

Capela, João Paulo; Ruscher, Karsten; Lautenschlager, Marion; Freyer, Dorette; Dirnagl, Ulrich; Gaio, Rita; Bastos, Maria de Lourdes; Meisel, Andreas; Carvalho, Félix

doi:10.1016/j.neuroscience.2006.01.007

Cited by 73 publications

(87 citation statements)

References 39 publications

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“…However, the neurotoxic effects of the drugs of abuse may be enhanced by environmental factors, such as elevated temperature and loud noise (Gesi et al, 2004;Capela et al, 2006b). In contrast, stress manipulations (e.g.…”

Section: 4mentioning

confidence: 99%

“…MDMA also induces apoptotic features in PC12 cells (Milhazes et al, 2006) and in rat cortical neurons (Capela et al, 2006b). MDMA-induced apoptosis in rat cortical neurons seems to be dependent on 5-HT 2A receptor activation (Capela et al, 2006b).…”

mentioning

confidence: 99%

“…MDMA-induced apoptosis in rat cortical neurons seems to be dependent on 5-HT 2A receptor activation (Capela et al, 2006b). …”

mentioning

confidence: 99%

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Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

198

136

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Section: 4mentioning

confidence: 99%

mentioning

confidence: 99%

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Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cunha‐Oliveira

Rego

Oliveira

2008

Brain Research Reviews

198

136

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“…At or above this level, MDMA did induce macrophage death, consistent with literature reports that other cell types exposed to high micromolar, or low millimolar concentrations of MDMA, resulted in cell death in vitro. The drug induces apoptosis in primary, cortical neuronal cultures (Capela et al, 2007;Capela et al, 2006;Stumm et al, 1999), cerebellar granule cells (Jimenez et al, 2004), the neuronal cell line, PC12 (Milhazes et al, 2006), choriocarcinoma placental (JAR) cells (Simantov and Tauber, 1997), rat primary hepatocytes (Montiel-Duarte et al, 2004;Montiel-Duarte et al, 2002) and hepatic stellate cells (Montiel-Duarte et al, 2004). The cytotoxicity of MDMA and its metabolites is reported to be by an oxidative mechanism (Milhazes et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

“…We have initiated a survey of the expression of monoamine transporters and receptors in mouse macrophages, and find, intriguingly, expression of the mRNA for serotonin receptor Htr2a (unpublished results). Binding of MDMA to this receptor has recently been coupled to apoptosis in cortical neurons (Capela et al, 2007;Capela et al, 2006), and may account for both macrophage immunomodulation and, at higher concentrations, cell death. Further studies will need to be performed to ascertain if this macrophage receptor mediates these effects following drug exposure.…”

Section: Discussionmentioning

confidence: 99%

Ecstasy (3,4-methylenedioxymethamphetamine) limits murine gammaherpesvirus-68 induced monokine expression

Nelson

Nirmaier

Singh

et al. 2008

Brain, Behavior, and Immunity

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While Ecstasy (3, 4-methylenedioxymethamphetamine, MDMA) has been shown to modulate immune responses, no studies have addressed drug-induced alterations to viral infection. In this study, bone marrow-derived macrophages were exposed to MDMA, then infected with murine gammaherpesvirus-68, and the expression of monokines assessed. MDMA-induced reductions in virus-stimulated monokine mRNA expression were observed in a dose-dependent manner. In particular, IL-6 mRNA expression and secretion was significantly decreased in gammaherpesvirus-infected macrophages exposed to MDMA. Concentrations of MDMA capable of reducing monokine production did not induce significant cell death and allowed normal viral gene expression. These studies represent the first to demonstrate the ability of this drug of abuse to alter a viral-induced macrophage response.

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In Vivo Imaging of Cerebral Serotonin Transporter and Serotonin2A Receptor Binding in 3,4-Methylenedioxymethamphetamine (MDMA or “Ecstasy”) and Hallucinogen Users

Erritzoe¹,

Frøkjær²,

Holst³

et al. 2011

Arch Gen Psychiatry

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We found evidence that MDMA but not hallucinogen use is associated with changes in the cerebral presynaptic serotonergic transmitter system. Because hallucinogenic drugs primarily have serotonin(2A) receptor agonistic actions, we conclude that the negative association between MDMA use and cerebral SERT binding is mediated through a direct presynaptic MDMA effect rather than by the serotonin(2A) agonistic effects of MDMA. Our cross-sectional data suggest that subcortical, but not cortical, recovery of SERT binding might take place after several months of MDMA abstinence.

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Ecstasy-induced cell death in cortical neuronal cultures is serotonin 2A-receptor-dependent and potentiated under hyperthermia

Cited by 73 publications

References 39 publications

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Cellular and molecular mechanisms involved in the neurotoxicity of opioid and psychostimulant drugs

Ecstasy (3,4-methylenedioxymethamphetamine) limits murine gammaherpesvirus-68 induced monokine expression

In Vivo Imaging of Cerebral Serotonin Transporter and Serotonin2A Receptor Binding in 3,4-Methylenedioxymethamphetamine (MDMA or “Ecstasy”) and Hallucinogen Users

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