Methylenedioxymethamphetamine-induced hyperthermia and neurotoxicity are independently mediated by 5-HT2 receptors

Schmidt, Christopher J.; Black, Christine K.; Abbate, Gina M.; Taylor, Vicki L.

doi:10.1016/0006-8993(90)90813-q

Cited by 119 publications

(61 citation statements)

References 12 publications

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“…neurotoxicity seems to do so by producing hypothermia (Bowyer et al, 1994). However, it is reported that treatment with reserpine, which produces hypothermia, does not prevent the neurotoxic effects of METH (Albers and Sonsalla, 1995) and that MDL27777, a selective 5-HT uptake inhibitor, does not alter methylenedioxymethamphetamine-induced hyperthermia but completely prevents the neurotoxicity to serotonergic neurons (Schmidt et al, 1990). These findings suggest that hyperthermia might contribute to, but cannot be the sole cause of, the neuropathology produced by amphetamines.…”

Section: Discussionmentioning

confidence: 99%

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Nakajima¹,

Yamada²,

Nagai³

et al. 2004

J. Neurosci.

164

155

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Section: Discussionmentioning

confidence: 99%

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Nakajima¹,

Yamada²,

Nagai³

et al. 2004

J. Neurosci.

164

155

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“…A problem in interpreting these data, however, is the fact that mazindol does have some serotonin reuptake inhibitory activity, although its activity at dopamine and noradrenaline sites is undoubtedly higher (Heikkila et al, 1981;Angel et al, 1988;Shimizu et al, 1992). Other compounds, such as 5-HT 2 receptor antagonists (MDL 11,939 or ritanserin) and MAO-B inhibitors (l-deprenyl or MDL-72974), have shown efficacy in preventing neuronal damage when administered within 1 h of MDMA (Schmidt et al, 1990b;Sprague and Nichols, 1995), but their effect on rectal temperature was not evaluated. 6.…”

Section: Studies On Neuroprotectionmentioning

confidence: 99%

The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”)

Green

Mechan

Elliott

et al. 2003

Pharmacological Reviews

1,107

1,198

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“…The 5-HT 2A receptor plays a role in the acute response to MDMA, with 5-HT 2A antagonists reducing the locomotor response to MDMA (Bankson and Cunningham, 2002;Kehne et al, 1996) and MDMA-induced hyperthermia Schmidt et al, 1990). A role for the 5-HT 2C receptor in acute MDMA effects is also suggested by the fact that a 5-HT 2C receptor antagonist potentiates MDMA-induced hyperactivity (Bankson and Cunningham, 2002).…”

Section: -Ht 2a/2c Receptor Bindingmentioning

confidence: 99%

Increased Anxiety 3 Months after Brief Exposure to MDMA (‘Ecstasy’) in Rats: Association with Altered 5-HT Transporter and Receptor Density

McGregor

Clemens

Plasse

et al. 2003

Neuropsychopharmacol

106

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Male Wistar rats were treated with 3,4-methylenedioxymethamphetamine (MDMA, 'Ecstasy') using either a high dose (4 Â 5 mg/kg over 4 h) or low dose (1 Â 5 mg/kg over 4 h) regimen on each of 2 consecutive days. After 10 weeks, rats were tested in the social interaction and emergence tests of anxiety. Rats previously given either of the MDMA dose regimens were significantly more anxious on both tests. After behavioral testing, and 3 months after the MDMA treatment, the rats were killed and their brains examined. Rats given the high-, but not the low-, dose MDMA treatment regimen exhibited significant loss of 5-hydroxytryptamine (5-HT) and 5-HIAA in the amygdala, hippocampus, striatum, and cortex. Quantitative autoradiography showed loss of SERT binding in cortical, hippocampal, thalamic, and hypothalamic sites with the high-dose MDMA regime, while low-dose MDMA only produced significant loss in the medial hypothalamus. Neither high-nor low-dose MDMA affected 5HT 1A receptor density. High-dose MDMA increased 5HT 1B receptor density in the nucleus accumbens and lateral septum but decreased binding in the globus pallidus, insular cortex and medial thalamus. Low-dose MDMA decreased 5HT 1B receptor density in the hippocampus, globus pallidus, and medial thalamus. High-dose MDMA caused dramatic decreases in cortical, striatal, thalamic, and hypothalamic 5HT 2A / 2C receptor density, while low-dose MDMA tended to produce similar effects but only significantly in the piriform cortex. These data suggest that even brief, relatively low-dose MDMA exposure can produce significant, long-term changes in 5-HT receptor and transporter function and associated emotional behavior. Interestingly, long-term 5-HT depletion may not be necessary to produce lasting effects on anxiety-like behavior after low-dose MDMA.

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Methylenedioxymethamphetamine-induced hyperthermia and neurotoxicity are independently mediated by 5-HT2 receptors

Cited by 119 publications

References 12 publications

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

Role of Tumor Necrosis Factor-α in Methamphetamine-Induced Drug Dependence and Neurotoxicity

The Pharmacology and Clinical Pharmacology of 3,4-Methylenedioxymethamphetamine (MDMA, “Ecstasy”)

Increased Anxiety 3 Months after Brief Exposure to MDMA (‘Ecstasy’) in Rats: Association with Altered 5-HT Transporter and Receptor Density

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