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ALTERATIONS IN PREFRONTAL CORTEX FUNCTION IN THE <EM>FMR1</EM>KO MOUSE MODEL OF AUTISM AND FRAGILE X SYNDROME
Melanie Gingerand 10 co-authors
Neurocentre Magendie
FENS Forum 2026 (2026)
Barcelona, Spain
Board PS02-07PM-320
Presentation
Date TBA
Board: PS02-07PM-320
Event Information
Poster Board
PS02-07PM-320
Poster
View posterAbstract
The Fmr1 knockout mouse is one of the most studied models of neurodevelopmental conditions and is considered a model for both fragile X syndrome and autism. These conditions are characterized by overlapping endophenotypes, such as attentional problems or difficulties with executive function that strongly implicate the prefrontal cortex (PFC). To study alterations in PFC function underlying these endophenotypes in Fmr1KO mice, we used trace fear conditioning combined with population calcium measurements using miniature micrsocope in freely moving, behaving mice. We found defects in the capacity of Fmr1KO mice to form a link between a pure tone and the unconditioned stimulus delivered after a 30 sec trace interval, while the processing of contextual cues, or the tone itself, was intact. These behavioural changes are accompanied by an alteration in the activity dynamics of the anterior cingulate cortex (ACC) circuits in these mice, and an absence of ACC disengagement during the later conditioning phases, which was observed in wild type mice. We currently explore mechanisms for these changes with a goal of identifying the cellular and circuit substrates of altered attentional processing in these mice.
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