CaV2.1 ablation in cortical interneurons selectively impairs fast‐spiking basket cells and causes generalized seizures
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Objective: Both the neuronal populations and mechanisms responsible for generalized spike‐wave absence seizures are poorly understood. In mutant mice carrying loss‐of‐function (LOF) mutations in Cacna1a,which encodes the α1 pore‐forming subunit of Ca V 2.1 (P/Q‐type) voltage‐gated Ca 2+channels, generalized spike‐wave seizures have been suggested to result from excessive bursting of thalamocortical cells. However, other cellular populations including cortical inhibitory interneurons may contribute to this phenotype. We investigated how different cortical interneuron subtypes are affected by the loss of Ca V 2.1 channel function and how this contributes to the onset of generalized epilepsy. Methods: We designed genetic strategies to induce a selective Cacna1a LOF mutation in different cortical γ‐aminobutyric acidergic (GABAergic) and/or glutamatergic neuronal populations in mice. We assessed the cellular and network consequences of these mutations by combining immunohistochemical assays, in vitro physiology, optogenetics, and in vivo video electroencephalographic recordings. Results: We demonstrate that selective Cacna1a LOF from a subset of cortical interneurons, including parvalbumin (PV)+and somatostatin (SST)+interneurons, results in severe generalized epilepsy. Loss of Ca V 2.1 channel function compromises GABA release from PV+but not SST+interneurons. Moreover, thalamocortical projection neurons do not show enhanced bursting in these mutants, suggesting that this feature is not essential for the development of generalized spike‐wave seizures. Notably, the concurrent removal of Ca V 2.1 channels in cortical pyramidal cells and interneurons considerably lessens seizure severity by decreasing cortical excitability. Interpretation: Our findings demonstrate that conditional ablation of Ca V 2.1 channel function from cortical PV+interneurons alters GABA release from these cells, impairs their ability to constrain cortical pyramidal cell excitability, and is sufficient to cause generalized seizures. Ann Neurol 2013;74:209–222
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The delay between the peak of an action potential in a FS basket cell soma and the start of the uIPSC in a postsynaptic pyramidal cell averages 0.7 ms at ~31°C, with jitter of 0.19 ms.
“The delay between the peak of an action potential in a FS basket cell soma and the start of the uIPSC in a postsynaptic pyramidal cell is on the average 0.7 ms (at ~31 °C) and the jitter between different responses 0.19 ms”
From GABAergic Interneurons in the Neocortex: From Cellular Properties to Circuits (2016) · cites this paper as Rossignol et al., 2013
The Results section on FS-interneuron GABA release reports uIPSCs in pyramidal cells and a 100 ± 12% increase in onset jitter in mutant mice. Searches for the stated latency, 0.19-ms jitter, and ~31°C condition found no passage in our copy giving those measurements. (LLM, conf=0.76)
Experimental — accuracy not yet measuredPV cINs exert strong inhibitory control over local networks and their dysfunction is implicated in Dravet syndrome, focal epilepsy, ASD, and schizophrenia.
“These neurons exert a strong level of inhibitory control over local networks and their disfunction has been directly implicated in neurological and neuropsychiatric disorders, including Dravet syndrome, focal epilepsy, ASD and schizophrenia 31–34.”
From Viral manipulation of functionally distinct interneurons in mice, non-human primates and humans (2020) · cites this paper as [32]
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- Authors
- Rossignol, E., Kruglikov, I., van den Maagdenberg, A. M. J. M., Rudy, B., & Fishell, G.
- Affiliations
- Centre Hospitalier Universitaire Sainte-Justine (CA)
- NYU Neuroscience Institute New York University School of Medicine New York NY
- Departments of Human Genetics and Neurology Leiden University Medical Center Leiden the Netherlands
- NYU Langone Health (US)
- Corresponding author
- Rudy, Bernardo
- Fishell, Gord
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2013-07
- Volume
- 74
- Issue
- 2
- Pages
- 209-222
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC3849346
- OpenAlex
- W1920656927
- Cited by
- 112
- References
- 72
- Citations by year
- 2026: 7 · 2025: 5 · 2024: 9 · 2023: 7 · 2022: 7 · 2021: 12 · 2020: 13 · 2019: 8 · 2018: 9 · 2017: 12 · 2016: 6 · 2015: 9 · 2014: 7 · 2013: 1
- FWCI
- 5.43
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Leiden Repository (Leiden University) (submittedVersion)
- Funders
- Simons Foundation
- National Institutes of Health (5r01ns030989-22)
- Canadian Institutes of Health Research
- National Institute of Mental Health (R01MH071679, R37MH071679)
- National Institute of Neurological Disorders and Stroke (R01-NS030989, P01NS074972, R01NS045217, R01NS039007, R01NS081297)
- 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
- P/Q-type calcium channels, CACNA1A, absence seizures, cortical interneurons, parvalbumin interneurons, somatostatin interneurons, GABA release, cortical excitability, pyramidal neurons, epilepsy, conditional gene deletion
- MeSH terms
- Animals, Cerebral Cortex, gamma-Aminobutyric Acid, Interneurons, Mice, Transgenic, Mutation, Parvalbumins, Phenotype, Seizures, Somatostatin, Calcium Channels, N-Type, Mice
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Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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