(developing a knockout mouse model for PD has been commented upon by a couple of neurologist as a very important part of the research for PD. Hope this model works.)
Neurology. 2006 Oct 10;67(7 Suppl 2):S12-7. Related Articles, Links


DDD mice, a novel acute mouse model of Parkinson's disease.

Sotnikova TD, Caron MG, Gainetdinov RR.

Department of Cell Biology and Center for Models of Human Disease, IGSP, Duke University Medical Center, Durham, North Carolina 27710, USA.

We describe the development of a novel animal model of acute severe dopamine (DA) deficiency by using genetically altered mice lacking the DA transporter (DAT-KO mice). In the absence of a DAT-mediated recycling mechanism in these mice, striatal DA concentrations become entirely dependent on its de novo synthesis, and acute pharmacologic inhibition of tyrosine hydroxylase induces transient (up to 16 hours) elimination of brain DA. Dopamine-deficient DAT-KO mice (DDD mice) demonstrate a striking behavioral phenotype manifested as severe akinesia, rigidity, tremor, and ptosis. We propose that DDD mice represent a novel acute model of severe DA deficiency that might be used to identify compounds with potential therapeutic use for the treatment of Parkinson's disease (PD). This model is particularly promising as a tool for evaluating the efficacy of compounds that may induce movement independently of DA. The advantages and limitations of DDD mice in comparison to other rodent PD models are discussed.

PMID: 17030735 [PubMed - in process]