| First Author | Cano-Jaimez M | Year | 2010 |
| Journal | Neurobiol Dis | Volume | 38 |
| Issue | 1 | Pages | 92-103 |
| PubMed ID | 20079841 | Mgi Jnum | J:159933 |
| Mgi Id | MGI:4453080 | Doi | 10.1016/j.nbd.2010.01.003 |
| Citation | Cano-Jaimez M, et al. (2010) Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by alpha-synuclein. Neurobiol Dis 38(1):92-103 |
| abstractText | 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. |
