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LOSS OF KCC2 IN INHIBITORY INTERNEURONS DISRUPTS CORTICAL DEVELOPMENT
Säde Loukasmäkiand 5 co-authors
University of Helsinki
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS05-09AM-456
Presentation
Date TBA
Board: PS05-09AM-456
Event Information
Poster Board
PS05-09AM-456
Poster
View posterAbstract
Previous research has established the importance of the expression of the neuronal chloride extruder KCC2 in principal neurons, highlighting its role in hyperpolarizing inhibition and for neurological development. However, the role of KCC2 expression in inhibitory interneurons and its implications to cortical development remain unclear. Inspired by our team’s recent finding that KCC2 is expressed remarkably early in a subset of early-maturing, somatostatin-expressing cortical interneurons, we aim to answer how interneuronal KCC2 expression shapes the development of cortical networks by selectively deleting it from this neuronal population. To this end, we developed a mouse model which has a conditional knock-out of KCC2 in the most prominent cortical interneuron types; somatostatin and parvalbumin interneurons. We used calcium imaging and extracellular recordings to study network activity of both inhibitory and excitatory networks, as well as immunohistochemical methods to assess network development during a critical period of activity-dependent somatosensory cortex maturation. Our preliminary findings suggest that KCC2 expression in inhibitory interneurons is necessary for normal neurological development. In the absence of KCC2 from interneurons, we see changes in the activity of inhibitory networks, cortical oscillations and laminar distribution of interneurons as well as spontaneous seizures.
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