These Pink1 (PTEN induced putative kinase 1) knockout mice have exons 4 through 7 deleted, disrupting most of the kinase domain and producing a nonsense mutation at the start of exon 8 due to a reading frame shift. Missense mutations in the PINK1 gene cause autosomal-recessive Parkinson's disease. PINK1 loss of function results in mitochondrial dysfunction, increased reactive oxygen species production and calcium homeostasis imbalance. Homozygous mutant mice are viable and fertile. No Pink1 mRNA is detected by Northern blot analysis in brain tissue from homozygotes. Evoked release of striatal dopamine and catecholamine, and catecholamine release by adrenal chromaffin cells is decreased in homozygotes. Dopamine levels in the striatum, dopaminergic neuron number, dopamine synthesis and dopamine receptor number are not altered. Homozygotes exhibit impaired induction of long-term potentiation and long-term depression at corticostriatal synapses. No nigrostriatal neurodegeneration is detected in homozygous mice 9 months of age. Homozygotes are more sensitive to metabotropic glutamate (mGlu) receptor agonist than wildtype controls.

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These Pink1 knockout mice exhibit reduced mean evoked dopamine overflow, altered dopamine signaling, and have applications in studies related to Parkinson's disease.

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