Journal
NEUROBIOLOGY OF DISEASE
Volume 38, Issue 1, Pages 92-103Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2010.01.003
Keywords
alpha-Synuclein knockout; Neurotrophic factor; Peripheral nervous system; Sympathetic nervous system; Autonomic ganglia; MPP+; Noradrenergic system; Cardiac innervation; Dopaminergic neuron; Substantia nigra
Categories
Funding
- Ministerio de Ciencia e Innovacion
- Ministerio de Sanidad y Consumo
- Generalitat Valenciana
- Fundacion la Caixa
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Although generally considered a prototypical movement disorder, Parkinson's disease is commonly associated with a broad-spectrum of non-motor symptoms, including autonomic dysfunctions caused by significant alterations in catecholaminergic neurons of the peripheral sympathetic nervous system. Here we present evidence that alpha-synuclein is highly expressed by sympathetic ganglion neurons throughout embryonic and postnatal life and that it is found in tyrosine hydroxylase-positive sympathetic fibers innervating the heart of adult mice. However, mice deficient in alpha-synuclein do not exhibit any apparent alterations in sympathetic development. Sympathetic neurons isolated from mouse embryos and early postnatal mice are sensitive to the parkinsonian drug MPTP/MPP+ and intoxication requires entry of the neurotoxin through the noradrenaline transporter. Furthermore, recovery of noradrenaline from cardiac sympathetic fibers is reduced in adult mice treated with MPTP systemically. However, MPP+-induced sympathetic neuron loss in vitro or MPTP-induced cardiac noradrenaline depletion in vivo is not modified in mice lacking alpha-synuclein. This is in clear contrast with the observation that dopaminergic neurons of the central nervous system are significantly less vulnerable to MPTP/MPP+ in the absence of alpha-synuclein, suggesting different actions of this molecule in central and peripheral catecholaminergic neurons. (C) 2010 Elsevier Inc. All rights reserved.
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