Neuropharmacology and neurotoxicity of 3,4-methylenedioxymethamphetamine.

Gary A. Gudelsky, Bryan Yamamoto

Research output: Contribution to journalReview article

42 Citations (Scopus)

Abstract

The existing data indicate that MDMA produces long-term deficits in markers of 5-HT axon terminals in the rodent brain. Increased cleavage of the cytoskeletal protein tau, impairment of axonal transport, and functional consequences associated with a 5-HT depleting regimen of MDMA support the view that MDMA induces structural brain damage, that is, axonal degeneration. A confluence of oxidative stress and bioenergetic stress induced by MDMA is hypothesized to underlie the process of MDMA neurotoxicity (Fig. 3). The actions of MDMA on the 5-HT transporter to promote free radical formation and/or intracellular calcium may synergize with MDMA-induced disturbances in cellular energetics and hyperthermia to effect selective toxicity to 5-HT axon terminals.

Original languageEnglish (US)
Pages (from-to)55-73
Number of pages19
JournalMethods in molecular medicine
Volume79
StatePublished - 2003
Externally publishedYes

Fingerprint

Neuropharmacology
N-Methyl-3,4-methylenedioxyamphetamine
Serotonin
Presynaptic Terminals
Axonal Transport
Cytoskeletal Proteins
Brain
Energy Metabolism
Free Radicals
Rodentia
Oxidative Stress
Fever
Calcium

Cite this

Neuropharmacology and neurotoxicity of 3,4-methylenedioxymethamphetamine. / Gudelsky, Gary A.; Yamamoto, Bryan.

In: Methods in molecular medicine, Vol. 79, 2003, p. 55-73.

Research output: Contribution to journalReview article

@article{adc283a4bed84af9a1501929799d96f6,
title = "Neuropharmacology and neurotoxicity of 3,4-methylenedioxymethamphetamine.",
abstract = "The existing data indicate that MDMA produces long-term deficits in markers of 5-HT axon terminals in the rodent brain. Increased cleavage of the cytoskeletal protein tau, impairment of axonal transport, and functional consequences associated with a 5-HT depleting regimen of MDMA support the view that MDMA induces structural brain damage, that is, axonal degeneration. A confluence of oxidative stress and bioenergetic stress induced by MDMA is hypothesized to underlie the process of MDMA neurotoxicity (Fig. 3). The actions of MDMA on the 5-HT transporter to promote free radical formation and/or intracellular calcium may synergize with MDMA-induced disturbances in cellular energetics and hyperthermia to effect selective toxicity to 5-HT axon terminals.",
author = "Gudelsky, {Gary A.} and Bryan Yamamoto",
year = "2003",
language = "English (US)",
volume = "79",
pages = "55--73",
journal = "Methods in molecular medicine",
issn = "1543-1894",
publisher = "Humana Press",

}

TY - JOUR

T1 - Neuropharmacology and neurotoxicity of 3,4-methylenedioxymethamphetamine.

AU - Gudelsky, Gary A.

AU - Yamamoto, Bryan

PY - 2003

Y1 - 2003

N2 - The existing data indicate that MDMA produces long-term deficits in markers of 5-HT axon terminals in the rodent brain. Increased cleavage of the cytoskeletal protein tau, impairment of axonal transport, and functional consequences associated with a 5-HT depleting regimen of MDMA support the view that MDMA induces structural brain damage, that is, axonal degeneration. A confluence of oxidative stress and bioenergetic stress induced by MDMA is hypothesized to underlie the process of MDMA neurotoxicity (Fig. 3). The actions of MDMA on the 5-HT transporter to promote free radical formation and/or intracellular calcium may synergize with MDMA-induced disturbances in cellular energetics and hyperthermia to effect selective toxicity to 5-HT axon terminals.

AB - The existing data indicate that MDMA produces long-term deficits in markers of 5-HT axon terminals in the rodent brain. Increased cleavage of the cytoskeletal protein tau, impairment of axonal transport, and functional consequences associated with a 5-HT depleting regimen of MDMA support the view that MDMA induces structural brain damage, that is, axonal degeneration. A confluence of oxidative stress and bioenergetic stress induced by MDMA is hypothesized to underlie the process of MDMA neurotoxicity (Fig. 3). The actions of MDMA on the 5-HT transporter to promote free radical formation and/or intracellular calcium may synergize with MDMA-induced disturbances in cellular energetics and hyperthermia to effect selective toxicity to 5-HT axon terminals.

UR - http://www.scopus.com/inward/record.url?scp=0037209051&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037209051&partnerID=8YFLogxK

M3 - Review article

VL - 79

SP - 55

EP - 73

JO - Methods in molecular medicine

JF - Methods in molecular medicine

SN - 1543-1894

ER -