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. 2018 Dec 6;19(12):3911. doi: 10.3390/ijms19123911

Table 1.

Circadian dysfunctions in mammalian Parkinson’s disease (PD) models.

Mammalian Models Intervention Animal Model Circadian Phenotype
ASO Overexpression of wt α-syn in all brain regions Mouse Fragmented circadian rhythms and a reduced firing rate of SCN neurons during the day [31]
MitoPark Deletion for mitochondrial transcription factor A in dopaminergic neurons Mouse Age-dependent rhythm decline and disturbed circadian activity rhythms under constant high light conditions [32]
MPTP-injection Intraperitoneally and subcutaneously [33]
Intraperitoneally [34]
Mouse No significant changes in circadian parameters [33,34]
Not specified [35] Mouse Reduced amplitude in locomotor rhythm; altered clock gene expression in the SCN [35]
Intravenously [36] Dog Circadian urine volume and vasopressin release alteration [36]
Intramuscular [37] Non-human Primates Loss of circadian locomotor activity in the absence of light/dark cues [37]
6-OHDA-injection Bilateral in the striatum [38] Rat Altered clock gene expression in the striatum [38]
Intracerebroventricular and unilateral infusion in medial forebrain bundle [39] Rat Disorganized wheel-running pattern in constant darkness and blunted PER2 expression rise in the dorsal striatum [39]
Bilateral in the ventral tegmental area [40] Rat Reduced locomotor activity period in LD and longer activity rhythm periodicity under constant dim light [40]
Bilateral in the striatum [41] Rat Decreased amplitude of the heart rate rhythm [41]
Bilateral in the striatum [42] Rat Altered clock gene expression profile in SNC and in the striatum [42]