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Evaluation of a Parkinson's disease model in medaka fish
Author(s) -
Ferng Shiana J.,
Gonzalez David E.,
Nguyen Mary N.,
Sherman Scott J.,
Falk Torsten,
Rilo Horacio L.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.567.1
Subject(s) - oryzias , zebrafish , substantia nigra , dopaminergic , neurotoxin , parkinson's disease , fish <actinopterygii> , dopamine , neuroscience , penetrance , biology , disease , pathology , physiology , medicine , endocrinology , phenotype , genetics , gene , fishery
Parkinson's disease (PD) is the 2nd most common neurodegenerative disease. Dopaminergic (DA) neurons in the substantia nigra of the brain are the most vulnerable to PD. 6‐ hydroxydopamine (6‐OHDA) is a neurotoxin structurally similar to dopamine that is transported inside the brain and destroys DA neurons. The resulting PD symptoms can be identified through behavioral analysis and verification of DA neuron loss through immunohistochemical analysis in medaka fish (Oryzias latipes). Medaka are well‐suited as a PD model because they are transparent during most stages of development, produce numerous offspring, and readily absorb toxicants through their skin. To establish a PD medaka model to time and cost‐efficiently screen drugs that may change the progression of PD, medaka were exposed to varying concentrations of 6‐OHDA through the water they swam in. Temporary acquired PD symptoms were evidenced by an initial decrease in total distance swam by 6‐OHDA‐treated medaka and changes in turn angle, but a complete behavioral recovery was evident at following time points. The results indicate that medaka exposure to 6‐OHDA in the water is not sufficient to induce loss of DA neurons, presumably due to a reduced blood‐brain barrier penetrance of 6‐OHDA in medaka as compared to the established zebrafish model. Support: Univ. of AZ (UA) from Howard Hughes Medical Inst. (#52006942); NIH NINDS 1R25NS076437; UA Dept. Neurology.