Pink1 (Park6) Knockout Rat
Model Detail >
- Parkinson's disease
- Stress-induced neurological dysfunction
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Developed in collaboration with The Michael J. Fox Foundation, this model contains a deletion of the Pink1 (PTEN-induced putative kinase 1) gene, encoding for a serine/threonine protein kinase. Mutations in Pink1 are implicated in early-onset Parkinson’s disease. Pink1 knockout rats show both motor impairments and dopaminergic cell loss, making this a useful model of Parkinson’s disease.
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Homozygous knockout rats exhibit complete loss of target protein
Approximately 30% of Pink1 knockout rats display a hindlimb-dragging phenotype at 5 months of age
Pink1 knockout rats show increased hindlimb fatigue at 7 weeks of age
Pink1 knockout rats show increased number of hindlimb foot slips at 5 and 9 weeks of age as assessed by tapered balance beam
Preliminary reports have suggested Pink1 knockout rats show a ~50% reduction in dopaminergic neurons in the substantia nigra at 8 months of age
Background Strain: Long Evans Hooded
Figure 1. Increased fatigue in Pink1 knockout rats
Pink1 homozygous and heterozygous knockout rats display decreased movement in an open field after hindlimb fatigue challenge, indicative of increased hindlimb fatigue.
Figure 2. Decreased performance on tapered balance beam in Pink1 knockout rats
Pink1 homozygous and heterozygous knockout rats display increased hindlimb foot slips on a tapered balance beam. No differences were seen in forelimb foot slips.
This model is being developed in partner with the Michael J. Fox Foundation as part of our Parkinson's disease research suite. Pink1 protein kinase localizes to the mitochondria and is thought to protect cells from stress-induced mitochondrial dysfunction. Mutations within this gene result in one form of autosomal recessive early-onset Parkinson's.