Direct central effects of acute methylenedioxymethamphetamine on serotonergic neurons

Schmidt, Christopher J.; Taylor, Vicki L.

doi:10.1016/0014-2999(88)90154-9

Cited by 84 publications

(51 citation statements)

References 22 publications

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“…For example, because direct infusion of MDMA into cerebroventricular space did not cause any toxicity, it was suggested that the neurodegenerative effects of the drug might be related to its metabolites. 29,33,40 This argument is supported, in part, by the demonstration that MDMA is metabolized into catechol and quinone metabolites. 29,33,40,44 Further metabolism of these compounds could result in the formation of free radicals which might induce oxidative stress, and subsequent cellular damage.…”

mentioning

confidence: 57%

“…29,33,40 This argument is supported, in part, by the demonstration that MDMA is metabolized into catechol and quinone metabolites. 29,33,40,44 Further metabolism of these compounds could result in the formation of free radicals which might induce oxidative stress, and subsequent cellular damage. 13 Other possible mechanisms also include: (i) increased metabolism of DA released by MDMA; 13,22,38 and (ii) formation of DA metabolites such as 6-hydroxydopamine which is known to cause oxidative stress.…”

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confidence: 57%

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Overexpression of human copper/zinc superoxide dismutase in transgenic mice attenuates oxidative stress caused by methylenedioxymethamphetamine (Ecstasy)

et al. 1999

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confidence: 57%

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confidence: 57%

Overexpression of human copper/zinc superoxide dismutase in transgenic mice attenuates oxidative stress caused by methylenedioxymethamphetamine (Ecstasy)

et al. 1999

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“…SERT has also been implicated in serotonin-mediated apoptosis in Burkitt's lymphoma 7 and in the mechanism of cytotoxicity associated with the amphetamine analogues, fenfluramine 8 and 3,4-methylenedioxymethamphetamine (MDMA) 9,10 . Although these ligands can target the serotonin transporter, their anticancer effects are thought to occur independently of SERT 1, 2, 11 suggesting that (a) molecular target(s) other than SERT may exist on the lymphoma cell with the possibility of these ligands preferentially targeting the proliferating malignant cell 1 .…”

Section: Introductionmentioning

confidence: 99%

Synthesis and serotonin transporter activity of 1,3-bis(aryl)-2-nitro-1-propenes as a new class of anticancer agents

McNamara¹,

Cloonan²,

Knox³

et al. 2011

Bioorganic & Medicinal Chemistry

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Synthesis and serotonin transporter activity of 1,3-bis(aryl)-2-nitro-1-propenes as a new class of anticancer agents, Bioorganic & Medicinal Chemistry (2010), doi: 10.1016/j.bmc.2010 This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. derived cell lines, whilst having no effect on 'normal' peripheral blood mononuclear cells. Such effects appear to be independent of the serotonin transporter, a high affinity target for amphetamines and independent of protein tyrosine phosphatases and tubulin dynamics both of which have been previously associated with nitrostyrene-induced cell death. We demonstrate that a number of these compounds induce caspase activation, PARP cleavage, chromatin condensation and membrane blebbing in a Burkitt's lymphoma-derived cell line, consistent with these compounds inducing apoptosis in vitro. Although no specific target has yet been identified for the action of these compounds, the cell death elicited is potent, selective and worthy of further investigation.

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“…Moderate to high doses of MDMA produce selective damage to 5-HT neurons as evidenced by the reduction of 5-HT transporter binding sites (Battaglia et al, 1987;Schmidt, 1987), 5-HT transporter immunoreactivity, (O'Hearn et al, 1988), and reductions of 5-HT content (Schmidt, 1987;O'Hearn et al, 1988) as well as tryptophan hydroxylase activity (Schmidt and Taylor, 1988). It follows that these deficits in mesolimbic 5-HT neurotransmission could alter the interaction of 5-HT with dopamine to affect the stimulant and rewarding effects of a subsequent MDMA administration.…”

Section: Introductionmentioning

confidence: 99%

Prior Exposure to Chronic Stress and MDMA Potentiates Mesoaccumbens Dopamine Release Mediated by the 5-HT1B Receptor

Amato

Bankson

Yamamoto

2006

Neuropsychopharmacol

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( + ) 3,4,-Methylenedioxymethamphetamine (MDMA) is an abused drug that acutely releases serotonin (5-HT) and dopamine (DA) but produces long-term damage to 5-HT terminals. MDMA-induced DA release has been shown to be dampened by 5-HT. Although stress also activates the mesolimbic DA pathway, it is unknown if chronic stress after exposure to neurotoxic doses of MDMA will augment MDMA-induced DA release in the nucleus accumbens shell (NAcc(sh)). Rats were pretreated with MDMA (10 mg/kg Â 4, intraperitoneal (i.p.)). After 7 days, rats were subjected to 10 days of chronic unpredictable stress. DA release in the NAcc(sh) and 5-HT in the ventral tegmental area (VTA) were measured after a challenge injection of MDMA (5 mg/kg, i.p.). The combination of pretreatment with MDMA + stress decreased basal concentrations of 5-HT in the VTA and DA in the NAcc(sh) and enhanced MDMAstimulated DA release in the NAcc(sh). Pretreatment with MDMA or stress alone blunted MDMA-induced 5-HT release in the VTA. The augmentation of MDMA-induced DA release in rats pretreated with MDMA + chronic stress was attenuated by perfusion of the 5-HT 1B antagonist, GR127935 into the VTA before the MDMA challenge injection. These results suggest that prior exposure to both MDMA and stress can produce a long-term augmentation in mesolimbic DA transmission and enhanced drug abuse vulnerability that is mediated, in part, by the 5-HT 1B receptor in the VTA. Neuropsychopharmacology (2007) 32, 946-954.

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Direct central effects of acute methylenedioxymethamphetamine on serotonergic neurons

Cited by 84 publications

References 22 publications

Overexpression of human copper/zinc superoxide dismutase in transgenic mice attenuates oxidative stress caused by methylenedioxymethamphetamine (Ecstasy)

Overexpression of human copper/zinc superoxide dismutase in transgenic mice attenuates oxidative stress caused by methylenedioxymethamphetamine (Ecstasy)

Synthesis and serotonin transporter activity of 1,3-bis(aryl)-2-nitro-1-propenes as a new class of anticancer agents

Prior Exposure to Chronic Stress and MDMA Potentiates Mesoaccumbens Dopamine Release Mediated by the 5-HT1B Receptor

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