View Full Text | Abstract |
Article as PDF | Print this Article |
Pubmed | PMC |
PubReader | Export to Citation |
Email Alerts | Open Access |
Exp Neurobiol 2012; 21(3): 94-100
Published online September 30, 2012
https://doi.org/10.5607/en.2012.21.3.94
© The Korean Society for Brain and Neural Sciences
Hideaki Matsui1*, Roberto Gavinio2 and Ryosuke Takahashi2*
1Department of Cell Physiology, Zoological Institute, Technical University Brauschweig, Braunschweig 38106, Germany, 2Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto 606-8507, Japan
Correspondence to: *To whom correspondence should be addressed.
Hideaki Matsui
TEL: 49-531-391-3235, FAX: 49-531-391-3222
e-mail: hide0729@kuhp.kyoto-u.ac.jp
Ryosuke Takahashi
TEL: 81-75-751-3770, FAX: 81-75-761-9780
e-mail: ryosuket@kuhp.kyoto-u.ac.jp
The teleost fish has been widely used in creating neurodegenerative models. Here we describe the teleost medaka fish Parkinson's disease (PD) models we developed using toxin treatment and genetic engineering. 1-Methyl-4-phenyl-1,2,3,4-tetrahydropyridine (MPTP), 6-hydroxydopamine (6-OHDA), proteasome inhibitors, lysosome inhibitors and tunicamycin treatment in our model fish replicated some salient features of PD: selective dopamine cell loss and reduced spontaneous movement with the last three toxins producing inclusion bodies ubiquitously in the brain. Despite the ubiquitous distribution of the inclusion bodies, the middle diencephalic dopaminergic neurons were particularly vulnerable to these toxins, supporting the idea that this dopamine cluster is similar to the human substantia nigra.
Keywords: Parkinson's disease, medaka fish, dopaminergic neurons, model animal