Study summary · research use only
A Role for Vasoactive Intestinal Peptide Interneurons in Neurodevelopmental Disorders
Plain-language summary
Paraphrased from the published abstract below — not a verdict on whether anything works.
This review article (species not specified) discusses the circuit functions of GABAergic cortical interneurons expressing vasoactive intestinal peptide (VIP-INs) and their reported involvement in neurodevelopmental disorders (NDDs). The authors describe recurring VIP-IN-mediated circuit patterns across cortical areas and how VIP-IN activity may relate to sensory input, development, and behavior. Using publicly available single-cell RNA sequencing data from the Allen Institute, the authors identify several underexplored disease-associated genes highly expressed in VIP-INs and describe related disease phenotypes, which they associate more with autism spectrum disorder and intellectual disability than with epileptic encephalopathy. The article concludes with discussion of the relevance of cell type-specific research and targeted therapeutics in genomic diagnosis.
Abstract
GABAergic inhibitory interneurons of the cerebral cortex expressing vasoactive intestinal peptide (VIP-INs) are rapidly emerging as important regulators of network dynamics and normal circuit development. Several recent studies have also identified VIP-IN dysfunction in models of genetically determined neurodevelopmental disorders (NDDs). In this article, we review the known circuit functions of VIP-INs and how they may relate to accumulating evidence implicating VIP-INs in the mechanisms of prominent NDDs. We highlight recurring VIP-IN-mediated circuit motifs that are shared across cerebral cortical areas and how VIP-IN activity can shape sensory input, development, and behavior. Ultimately, we extract a set of themes that inform our understanding of how VIP-INs influence pathogenesis of NDDs. Using publicly available single-cell RNA sequencing data from the Allen Institute, we also identify several underexplored disease-associated genes that are highly expressed in VIP-INs. We survey these genes and their shared related disease phenotypes that may broadly implicate VIP-INs in autism spectrum disorder and intellectual disability rather than epileptic encephalopathy. Finally, we conclude with a discussion of the relevance of cell type-specific investigations and therapeutics in the age of genomic diagnosis and targeted therapeutics.
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