General Information
Mouse: C57BL/6 x 129/Sv
Mice with a germ-line deletion of exons 4-7 of the PINK1 gene leading to non-sense mediated decay of truncated mRNA and no detectable expression of the PINK1 protein.
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: Kitada 2007
Neurodegeneration
- 2-9 months: normal morphology and no loss of TH-positive neurons are observed in the SN
Dopamine Homeostasis
- 2-9 months: no changes in the levels of dopamine and dopamine metabolites are observed in the striatum.
Inclusions
- Not reported
Motor Behaviours
- Not reported
Response to dopaminergic treatment
- Not reported
Non motor Behaviours
- Not reported
Electrophysiology
- 2-9 months: amperometric recordings indicate a significant decrease in electrical stimulation-evoked dopamine overflow which is due to reduced release of dopamine. This reflects a functional defect but not a structural defect as DNA synthesis and the number of TH-neurons is not affected.
- 2-9 months: Reduction of LTP and LTD is detected at cortical synapses; no alterations in synaptic plasticity are observed at hippocampal glutamatergic synapses.
Neuroinflammation
- Not reported