Skip to main content

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