Kinetics of alpha-synuclein depletion in three brain regions following conditional pan-neuronal inactivation of the encoding gene (Snca) by tamoxifen-induced Cre-recombination in adult mice.
Kirill D ChaprovEkaterina A LysikovaEkaterina V TeterinaVladimir L BuchmanPublished in: Transgenic research (2021)
Conditional pan-neuronal inactivation of the Snca gene in 2-month old male and female mice causes dramatic decrease in the level of the encoded protein, alpha-synuclein, in three studied brain regions, namely cerebral cortex, midbrain and striatum, 12 weeks after the last injection of tamoxifen. Kinetics of alpha-synuclein depletion is different in these brain regions with a longer lag period in the cerebral cortex where this protein is normally most abundant. Our results suggest that efficient post-developmental pan-neuronal knockout of alpha-synuclein in adult, i.e. 5- to 6-month old, animals, could be achieved by tamoxifen treatment of 2-month old mice carrying loxP-flanked Snca gene and expressing inducible Cre-ERT2 recombinase under control of the promoter of neuron-specific enolase (NSE) gene.
Keyphrases
- cerebral ischemia
- resting state
- copy number
- genome wide
- functional connectivity
- subarachnoid hemorrhage
- white matter
- genome wide identification
- high fat diet induced
- dna methylation
- breast cancer cells
- positive breast cancer
- wild type
- dna damage
- brain injury
- blood brain barrier
- oxidative stress
- type diabetes
- gene expression
- high glucose
- metabolic syndrome
- protein protein
- young adults
- insulin resistance
- multiple sclerosis
- adipose tissue