NDLI: D1 but not D4 Dopamine Receptors are Critical for MDMA-Induced Neurotoxicity in Mice

Content Provider	Springer Nature Link
Author	Granado, N. Ares Santos, S. Moratalla, R.
Copyright Year	2013
Abstract	MDMA, an addictive psychostimulant-consumed worldwide, has the ability to induce neurotoxic effects and addiction in laboratory animals and in humans through its effects on monoaminergic systems. MDMA-induced neurotoxicity in mice occurs primarily in dopaminergic neurons and does not significantly affect the serotonergic system. As the neurotoxic effects of MDMA in mice involve excessive dopamine (DA) release, DA receptors are highly likely to play a role in MDMA neurotoxicity, but the specific dopamine receptor subtypes involved have not previously been determined definitively. In this study, dopamine D1 and D4 receptor knock-out mice (D1R$^{−/−}$ and D4R$^{−/−}$) were used to determine whether these receptors are involved in MDMA neurotoxicity. D1R inactivation attenuated MDMA-induced hyperthermia, decreased the reduction of dopamine and dopamine metabolite levels, and protected against dopamine terminal loss and reactive astrogliosis as determined in the striatum, 7 days after MDMA treatment. In sharp contrast, inactivation of D4R did not prevent hyperthermia or the neurotoxic effects of MDMA. Altogether, these results indicate that D1R, but not D4R, plays a significant role in the dopaminergic striatal neurotoxicity observed after exposure to MDMA.
Starting Page	100
Ending Page	109
Page Count	10
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	25
Issue Number	1
e-ISSN	14763524
Language	English
Publisher	Springer US
Publisher Date	2013-11-21
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Amphetamine derivatives Methamphetamine Methcathinone DAT Drug addiction Parkinson’s disease Striatum TH Neurosciences Neurology Neurochemistry Pharmacology/Toxicology Neurobiology Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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