Table 3.

Parkin deficiency in mice with deletion of exon 3

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]

DA dopamine; DOPAC 3,4-dihydroxyphenylacetic acid; HVA homovanillic acid