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Table 3 Parkin deficiency in mice with deletion of exon 3

From: Multitasking guardian of mitochondrial quality: Parkin function and Parkinson’s disease

Unchanged parameters Observed changes
Viability [163, 164]
Fertility [163, 164]
Normal body mass [164, 167]
Normal general appearance [163, 164]
Normal brain morphology [163, 164, 167]
No brain inclusions [163]
No DA neuron loss in SN [163, 164, 167], striatum [164], and locus coeruleus [167]
Similar levels of DA, DOPAC and HVA in striatum [163]
Similar DA uptake in striatum [163, 171]
Similar D1 and D2 receptor binding in striatum [163, 171]
No muscle degeneration [164]
Normal rotarod performance [163, 167]
Normal long-term potentiation in hippocampus [164, 171]
Increased extracellular DA concentration in striatum [163]
Increased endogenous DA level in limbic region [164]
Reduced levels of DAT and VMAT2 in striatum [164]
Reduced synaptic excitability of medium-sized spiny striatal neurons [163]
Decreased DA release [171] vs increased DA release in striatum [169]
Decreased long-term potentiation in hippocampus [169]
Slightly increased paired-pulse facilitation in hippocampus [164]
Impaired long-term depression and long-term potentiation in striatum [171]
Worse beam traversal task performance [163]
Reduced exploratory behaviour [164, 167, 169]
Moderate impairment of spatial learning [167]
Increased anxiety (light / dark transition test) [167]
Decreased recognition index (object location task) [169]
Impaired spatial recognition memory (modified Y-maze task) [169]
  1. DA dopamine; DOPAC 3,4-dihydroxyphenylacetic acid; HVA homovanillic acid