J
Jon E. Sprague
Researcher at Bowling Green State University
Publications - 94
Citations - 2397
Jon E. Sprague is an academic researcher from Bowling Green State University. The author has contributed to research in topics: MDMA & Methylone. The author has an hindex of 26, co-authored 86 publications receiving 2210 citations. Previous affiliations of Jon E. Sprague include University of Manchester & Ohio Northern University.
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Journal Article
An integrated hypothesis for the serotonergic axonal loss induced by 3,4-methylenedioxymethamphetamine.
TL;DR: There is no clear evidence that human users of the street drug 3,4-methylenedioxymethamphetamine (MDMA) are suffering a similar neurotoxicity, but data are presented suggesting that there remains cause for concern.
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Pharmacology: uncoupling the agony from ecstasy.
TL;DR: The authors showed that mice deficient in a mitochondrial protein known as UCP-3 (for "uncoupling protein-3") have a diminished thermogenic response to the drug MDMA (3,4-methylenedioxymethamphetamine, nicknamed "ecstasy") and so are protected against this dangerous side effect.
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Synthetic cathinones ("bath salts").
TL;DR: Treatment of patients presenting after using bath salts should be focused on reducing agitation and psychosis and supporting renal perfusion, according to the majority of successfully treated synthetic cathinones cases.
Journal Article
The monoamine oxidase-B inhibitor L-deprenyl protects against 3,4-methylenedioxymethamphetamine-induced lipid peroxidation and long-term serotonergic deficits.
Jon E. Sprague,David E. Nichols +1 more
TL;DR: The data suggest that the deamination by monoamine oxidase-B of excessive dopamine within the 5-HT terminal generates hydrogen peroxide that may lead to membrane lipid peroxidation, and perhaps other oxidative insults, resulting in selective 5- HT terminal degeneration subsequent to MDMA treatment.
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Hypothalamic-Pituitary-Thyroid Axis and Sympathetic Nervous System Involvement in Hyperthermia Induced by 3,4-Methylenedioxymethamphetamine (Ecstasy)
TL;DR: The mechanisms of thermogenesis induced by MDMA seem to result from an interaction between the hypothalamic-pituitary-thyroid axis and the sympathetic nervous system, wherein mechanisms leading to core and skeletal muscle hyperthermia after MDMA exposure seem to be differentially regulated by α1- and β3-adrenergic receptors.