Loss of the neuronal kinase DCLK3 leads to anxiety-like behaviour and memory deficits

de Longprez L
February 5, 2025
Brain
https://pubmed.ncbi.nlm.nih.gov/39908340

This article is currently being updated. View its version on PubMed.

https://pubmed.ncbi.nlm.nih.gov/39908340

Research summary

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.

Key outcome of the study

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.

Mouse model

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.

TARGET:
Dclk3
Doublecortin-like kinase 3

Keywords

Neuroscience, Anxiety disorders, Memory deficits, Synaptic plasticity, Kinase function

Technical specifications

Constitutive Knockout, Region-specific Knockout, Cre-loxP system, Viral vector-mediated gene deletion, Behavioral phenotyping

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