Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines.

Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Research Abstract Details 

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Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Abstract Text:

Tao Xie,Liqiong Tong,Michael W McLane,George Hatzidimitriou,Jie Yuan,Una McCann,George Ricaurte,Tao Xie,Liqiong Tong,Michael W McLane,George Hatzidimitriou,Jie Yuan,Una McCann,George Ricaurte,

We studied in vivo expression of the serotonin transporter (SERT) protein after 3,4-methylenedioxymethamphetamine (MDMA), p-chloroamphetamine (PCA), or fenfluramine (FEN) treatments, and compared the effects of substituted amphetamines to those of 5,7-dihydroxytryptamine (5,7-DHT), an established serotonin (5-HT) neurotoxin. All drug treatments produced lasting reductions in 5-HT, 5-HIAA, and [(3)H]paroxetine binding, but no significant change in the density of a 70 kDa band initially thought to correspond to the SERT protein. Additional Western blot studies, however, showed that the 70 kDa band did not correspond to the SERT protein, and that a diffuse band at 63-68 kDa, one that had the anticipated regional brain distribution of SERT protein (midbrain>striatum>neocortex>cerebellum), was reduced after 5,7-DHT and was absent in SERT-null animals, was decreased after MDMA, PCA, or FEN treatments. In situ immunocytochemical (ICC) studies with the same two SERT antisera used in Western blot studies showed loss of SERT-immunoreactive (IR) axons after 5,7-DHT and MDMA treatments. In the same animals, tryptophan hydroxylase (TPH)-IR axon density was comparably reduced, indicating that serotonergic deficits after substituted amphetamines differ from those in SERT-null animals, which have normal TPH levels but, in the absence of SERT, develop apparent neuroadaptive changes in 5-HT metabolism. Together, these results suggest that lasting serotonergic deficits after MDMA and related drugs are unlikely to represent neuroadaptive metabolic responses to changes in SERT trafficking, and favor the view that substituted amphetamines have the potential to produce a distal axotomy of brain 5-HT neurons.

Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Publishing Authors By Initials

T Xie,L Tong,MW McLane,G Hatzidimitriou,J Yuan,U McCann,G Ricaurte,T Xie,L Tong,MW McLane,G Hatzidimitriou,J Yuan,U McCann,G Ricaurte,

For similar organic chemicals: amines: ethylamines: phenethylamines: amphetamines: p-chloroamphetamine research abstracts see: organic chemicals: amines: ethylamines: phenethylamines: amphetamines: p-chloroamphetamine research

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Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Neuropsychopharmacology : official publication of

VOLUME: 31

Page Numbers: 2639-51

Journal Abbreviation: Neuropsychopharmacology

ISSN: 0893-133X

DAY: 25

MONTH: 01

YEAR: 2006

Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 8904907

Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Keywords Mesh Terms:

KEYWORDS: p-Chloroamphetamine

MESH TERMS: toxicity

Chemical & Substance for Abstract: Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines. Information

Substance Name: Tryptophan Hydroxylase

Registry Number: EC 1.14.16.4

Grant and Affiliation Information for Loss of serotonin transporter protein after MDMA and other ring-substituted amphetamines.

AFFILIATION: Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21224, USA.

Country: United States

AGENCY: United States NIDA

GRANT: DA13790

ACRONYM: DA

MEDLINETA: Neuropsychopharmacology

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