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Dopamine D2 receptor dysfunction is rescued by adenosine A2A receptor antagonism in a model of DYT1 dystonia.

Abstract：

:DYT1 dystonia is an inherited disease linked to mutation in the TOR1A gene encoding for the protein torsinA. Although the mechanism by which this genetic alteration leads to dystonia is unclear, multiple lines of clinical evidence suggest a link between dystonia and a reduced dopamine D2 receptor (D2R) availability. Based on this evidence, herein we carried out a comprehensive analysis of electrophysiological, behavioral and signaling correlates of D2R transmission in transgenic mice with the DYT1 dystonia mutation. Electrophysiological recordings from nigral dopaminergic neurons showed a normal responsiveness to D2-autoreceptor function. Conversely, postsynaptic D2R function in hMT mice was impaired, as suggested by the inability of a D2R agonist to re-establish normal corticostriatal synaptic plasticity and supported by the reduced sensitivity to haloperidol-induced catalepsy. Although an in situ hybridization analysis showed normal D1R and D2R mRNA expression levels in the striata of hMT mice, we found a significant decrease of D2R protein, coupled to a reduced ability of D2Rs to activate their cognate Go/i proteins. Of relevance, we found that pharmacological blockade of adenosine A2A receptors (A2ARs) fully restored the impairment of synaptic plasticity observed in hMT mice. Together, our findings demonstrate an important link between torsinA mutation and D2R dysfunction and suggest that A2AR antagonism is able to counteract the deficit in D2R-mediated transmission observed in mutant mice, opening new perspectives for the treatment of this movement disorder.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Napolitano F,Pasqualetti M,Usiello A,Santini E,Pacini G,Sciamanna G,Errico F,Tassone A,Di Dato V,Martella G,Cuomo D,Fisone G,Bernardi G,Mandolesi G,Mercuri NB,Standaert DG,Pisani A

doi

10.1016/j.nbd.2010.03.003

subject

Has Abstract

pub_date

2010-06-01 00:00:00

pages

434-45

issue

3

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(10)00064-1

journal_volume

38

pub_type

杂志文章

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