Vasoactive intestinal peptide-expressing interneurons are impaired in a mouse model of Dravet syndrome
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Dravet Syndrome (DS) is a severe neurodevelopmental disorder caused by pathogenic loss of function variants in the gene SCN1A which encodes the voltage gated sodium (Na+) channel subunit Nav1.1. GABAergic interneurons expressing parvalbumin (PV-INs) and somatostatin (SST-INs) exhibit impaired excitability in DS (Scn1a+/-) mice. However, the function of a third major class of interneurons in DS – those expressing vasoactive intestinal peptide (VIP-IN) –is unknown. We recorded VIP-INs in brain slices from Scn1a+/-mice and wild-type littermate controls and found prominent impairment of irregular spiking (IS), but not continuous adapting (CA) VIP-INs, in Scn1a+/- mice. Application of the Nav1.1-specific toxin Hm1a rescued the observed deficits. The IS vs. CA firing pattern is determined by expression of KCNQ channels; IS VIP-INs switched to tonic firing with both pharmacologic blockade of M-current and muscarinic acetylcholine receptor activation. These results show that VIP-INs express Nav1.1 and are dysfunctional in DS, which may contribute to DS pathogenesis.
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Scn1a encodes Nav1.1, a sodium channel expressed in three non-overlapping neuronal populations: PV cINs, VIP cINs, and layer 5 pyramidal neurons.
“Scn1a encodes for Nav1.1, a sodium channel expressed in three non-overlapping neuronal populations: fast-spiking cortical interneurons expressing parvalbumin (PV cINs), dis-inhibitory cortical interneurons expressing the vaso-intestinal peptide (VIP cINs) and layer 5 pyramidal neurons14–16.”
From Viral manipulation of functionally distinct interneurons in mice, non-human primates and humans (2020) · cites this paper as [16]
Loss of Scn1a expression is especially associated with PV cIN dysfunction.
“As loss of expression of Scn1a is especially associated with PV cIN disfunction15–19”
From Viral manipulation of functionally distinct interneurons in mice, non-human primates and humans (2020) · cites this paper as [16]
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- Authors
- Goff, K. M., & Goldberg, E. M.
- Affiliations
- University of Pennsylvania (US)
- Children's Hospital of Philadelphia (US)
- Corresponding author
- Goldberg, Ethan M
- Venue
- eLife
- Publisher
- eLife Sciences Publications, Ltd
- Published
- 2019-07-08
- Volume
- 8
- ISSN
- 2050-084X (ISSN-L)
- PMC
- PMC6629374
- OpenAlex
- W2958569275
- Cited by
- 93
- References
- 63
- Citations by year
- 2026: 3 · 2025: 13 · 2024: 16 · 2023: 16 · 2022: 20 · 2021: 15 · 2020: 7 · 2019: 2
- FWCI
- 8.74
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- eLife (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- National Institute of Neurological Disorders and Stroke (K08 NS097633, R01 NS110869)
- Burroughs Wellcome Fund (Career Award for Medical Scientists)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Epilepsy research and treatment
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion channel regulation and function
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- Dravet syndrome, vasoactive intestinal peptide interneurons, SCN1A, Nav1.1 sodium channel, KCNQ channels, M-current, muscarinic receptors, GABAergic interneurons, neuronal excitability
- MeSH terms
- Action Potentials, Animals, Brain, Epilepsies, Myoclonic, Interneurons, Mice, Inbred C57BL, Mice, Transgenic, Vasoactive Intestinal Peptide, Mice, Knockout, Mice, 129 Strain, NAV1.1 Voltage-Gated Sodium Channel
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