PINK1-null (Pink1 -/-) – Mouse

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
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