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General Information
Mouse: C57BL/6 x 129/SvEvBrd
Mice in which exons 4-5 of the PINK1 gene have been deleted by insertion of a neo probe (PGK-neo-pA) using homologous recombination. This insertion removes the N-terminal portion of the PINK1 protein that contains the kinase activity causing loss of function.
Corresponding human genotype: Autosomal recessive mutation in the PINK1 gene causing a loss-of-function of the protein and leading to early-onset Parkinson’s disease (PARK6).
Mutated gene: PINK1
References: Akundi 2011
Loss of dopaminergic neurons
- 12 months: apparent reduction in the number of TH-positive neurons in the SN. This decrease is accompanied by an increase of phosphorylated c-Jun protein in dopaminergic neurons.
Dopamine Homeostasis
- 2 months: no changes in dopamine levels and dopamine turnover are detected in the striatum
- 6–12 months: reduction of dopamine levels in the striatum (levels are about 75% those measured in wild type mice). An increase in dopamine turnover is detected in the striatum.
Inclusions
- Not reported
Motor Behaviours
- Not reported
Response to dopaminergic treatment
- Not reported
Non motor Behaviours
- Not reported
Electrophysiology
- Not reported
Neuroinflammation
6 months: increased levels of cytokine (IL-1beta, IL-10 and IL-12) in the striatum in response to a peripheral inflammatory stimuli (LPS) suggesting an enhanced susceptibility to inflammation.