Lack of Parvalbumin leading to autism behaviors in mice

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.