Lack of Parvalbumin leading to autism behaviors in mice
DOI:
https://doi.org/10.54097/tkxbp203Keywords:
Autism Spectrum Disorder; Parvalbumin; Inhibitory Interneurons.Abstract
This literature review examines the role of parvalbumin (PV)-expressing interneurons in the development of autism spectrum disorder (ASD), emphasizing the critical impact of PV deficits on the balance between excitatory and inhibitory (E/I) neural transmissions. PV neurons play a key role in maintaining this balance, and their deficit leads to increased inhibitory synaptic transmission and disrupts the E/I equilibrium. This disruption is linked to core ASD-like behaviors in mouse models, including social interaction deficits, communication impairments, and altered sensory processing. These findings suggest that targeting PV expression may offer a potential therapeutic approach for mitigating ASD symptoms.
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