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DYSREGULATION OF SK AND KV2.1 POTASSIUM CHANNELS ACROSS BRAIN REGIONS IN THE RNLS8 MOUSE MODEL OF ALS-FTD
Teresa Garrettand 5 co-authors
Wright State University
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-250
Presentation
Date TBA
Board: PS05-09AM-250
Event Information
Poster Board
PS05-09AM-250
Poster
View posterAbstract
Frontotemporal dementia (FTD) is a frequent comorbidity in Amyotrophic Lateral Sclerosis (ALS), with up to 50% of ALS patients meeting the diagnostic criteria for FTD. Both conditions are linked by the pathological cytoplasmic aggregation of the protein TDP-43 and its subsequent depletion from the neuronal nucleus. This study aims to characterize changes in SK2, SK3, and Kv2.1 ion channels across multiple brain regions in the rNLS8 mouse model to better understand the mechanisms underlying altered neuronal excitability in the ALS-FTD spectrum. The rNLS8 model develops somatic TDP-43 inclusions in both the spinal cord and brain, providing an ideal platform to evaluate these comorbid disorders. Using immunohistochemistry and confocal imaging, we assessed the expression of SK2, SK3, Kv2.1, and NeuN in the prefrontal cortex (PFC), caudate nucleus, dentate gyrus, and CA1 of the hippocampus. Symptomatic and asymptomatic mice of both sexes were evaluated to determine the progression of potassium channel dysregulation and identify potential sex differences. Analysis included total fluorescence intensity alongside 3D neuronal reconstruction to quantify channel density specifically on the soma. Given that SK channels modulate the afterhyperpolarization (AHP) phase and firing frequency, and Kv2.1 is a critical determinant of intrinsic excitability, alterations in these colocalized channels would indicate significant impairment in neuronal firing patterns. These data may highlight novel therapeutic targets for treating the cognitive and behavioral components of FTD.
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