Study type: In vivo/preclinical · Status: Verified against declared source
VIP interneuron impairment promotes in vivo circuit dysfunction and autism-related behaviors in Dravet syndrome.
Cell reports · 2023
Study scale: Baseline activity levels during quiet rest measured by deconvolved event frequency were similar between genotypes (Figure S3), indicating that VIP-IN dysfunction in Scn1a+/− mice is state dependent.
Abstract only: Open source record
Product or molecular entity relationships
- VIP: Exact entity relationship. Legacy citation custody associates this source with the catalog record; no product-relevance conclusion is implied.
Plain-language verified summary
Question
The increase of VIP-IN and pyramidal neuron activity during locomotion reported by GCaMP7s fluorescence was quantified as a locomotion modulation index (MI) (STAR Methods),33 which was reduced in Scn1a+/− mice compared with age-matched WT littermates (Figures 2C–2F; VIP-INs −0.11 ± 0.04, p = 0.01; non-VIP neurons −0.16 ± 0.05, p = 0.005).
Methods
The increase of VIP-IN and pyramidal neuron activity during locomotion reported by GCaMP7s fluorescence was quantified as a locomotion modulation index (MI) (STAR Methods),33 which was reduced in Scn1a+/− mice compared with age-matched WT littermates (Figures 2C–2F; VIP-INs −0.11 ± 0.04, p = 0.01; non-VIP neurons −0.16 ± 0.05, p = 0.005).
Scale or participants
Baseline activity levels during quiet rest measured by deconvolved event frequency were similar between genotypes (Figure S3), indicating that VIP-IN dysfunction in Scn1a+/− mice is state dependent.
Key findings
All cerebral cortex interneurons form inhibitory connections with other interneurons, and VIP-INs also inhibit pyramidal cells.
Limitations and uncertainty
Cerebral cortex interneurons (INs) constitute a diversity of cell types defined by electrical activity, molecular profiles, anatomy, and patterns of connectivity, and are key components of the microcircuit functions that underlie behavior.1,2 IN dysfunction is also implicated in the pathogenesis of a range of neurological and psychiatric disorders including epilepsy, schizophrenia, and autism spectrum disorder (ASD).3,4 However, it remains unclear how subtype-specific IN dysfunction contributes to disorders defined by paroxysmal events (seizures) as well as durable impairments in cognitive function.
Verified against declared source. Verification is limited to the declared source and review scope. It does not mean independent replication or establish efficacy, safety, or suitability.