Authors:

Paige Edens

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About Paper:

Visual familiarity leads to the emergence of theta oscillations in the mouse primary visual cortex (V1). These oscillations are impaired in a model of Fragile X (FX) syndrome. However, the underlying mechanism of this impairment is not well understood. Parvalbumin-positive (PV) interneurons play a critical role in regulating the excitatory/inhibitory balance and the generation of theta oscillations. To understand the role of PV interneurons in visual processing and to determine the underlying cause of learning disability in FX, we studied the visual learning behavior of Fmr1 knockout mice (a model of FX syndrome), wild-type (WT) mice and Fmr1cON/PV- Cre mice, where the Fmr1 gene expression is rescued conditionally only in PV interneurons. While being blinded to their genotypes, a total of 20 mice were water restricted and trained in 4 stages to a Go/No-Go active visual discrimination task. Training scores were calculated based on the percent of correct trials (Hits and Correct Rejection) and percent of incorrect trials (False Alarm and Misses) to analyze the behavior. We found that WT had the highest training score, Fmr1 KO had the lowest training score, and Fmr1cON/PV-Cre had an intermediate score. A significant restoration in performance indicates that PV interneurons may play a critical role in visual processing and memory and underly the learning disability present in FX. These results provide an exciting avenue for future therapeutic treatments that focus on restoring the network impairments in the disorder rather than the resulting symptoms.

Source:

Purdue University / 2023

Topics:

No topics listed

Co-authors:

Paige Edens