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. 2023 May 18;44(3):559–576. doi: 10.24272/j.issn.2095-8137.2022.406

Table 1. Pathological and behavioral characterization of Pink1 KO mice.

PINK1 KO DAergic neurons Mitochondria Motor deficits Other phenotypes References
N/A: Not available. DAergic: Dopaminergic. DA: Dopamine. SNpc: Substantia nigra pars compacta.
Deletion of exons 4–7 Unchanged DA numbers and levels of striatal DA/DA receptor N/A N/A Striatal plasticity impairments; Increased excitatory transmission Feligioni et al., 2016; Kitada et al., 2007
Germline deletion N/A Impaired mitochondrial respiration in striatum; Increased larger mitochondria N/A Reduced aconitase activity Gautier et al., 2008
Deletion of exons 4–5 Loss of DA neurons in striatum; impaired DA release Altered mitochondrial calcium storage N/A Aberrant innate immune response Akundi et al., 2011
Deletion of exons 2–3 No DA neuronal neurodegeneration Increased mitochondrial fragmentation No motor deficits observed Serotonergic neuronal loss Glasl et al., 2012
G309D-PINK1 mutation Deficiency of striatal DA, no neurodegeneration Increased mitochondrial dysfunction with impaired mitochondrial fission Reduction of locomotor activity Absence of Lewy bodies in SNpc Gispert et al., 2009
Deletion of exon 1 N/A Fragmentation of mitochondria; Increased ROS level; Impaired mitochondrial ATP synthesis N/A Impaired calcium homeostasis Oliveras-Salvá et al., 2014
Deletion of exons 2–3 Reduction of DA in SNpc with neurodegeneration Increased mitochondrial stress Impaired motor abilities N/A Moisoi et al., 2014