This study investigates the role of Doublecortin-like kinase 3 (DCLK3), a kinase preferentially expressed in neurons, in regulating behavior and cognition. The research explores how the loss of DCLK3 affects anxiety-like behavior, memory performance, and associated molecular changes in the brain.
Constitutive deletion of Dclk3 resulted in increased anxiety-like behavior in male mice without significant motor or memory deficits. In contrast, region-specific Knockout of Dclk3 in the dorsal hippocampus led to spatial memory impairments and altered expression of genes associated with neuronal activity and synaptic plasticity.
The study utilized both constitutive and brain-region-specific Dclk3 Knockout mouse models. The constitutive Knockout mice had the Dclk3 gene globally deleted, while the brain-region-specific Knockout was achieved through virally mediated Cre recombinase expression, allowing for targeted deletion of Dclk3 in specific brain regions such as the dorsal hippocampus.
Neuroscience, Anxiety disorders, Memory deficits, Synaptic plasticity, Kinase function
Constitutive Knockout, Region-specific Knockout, Cre-loxP system, Viral vector-mediated gene deletion, Behavioral phenotyping
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