ArticleMolecular psychiatry2017
Ankyrin-G isoform imbalance and interneuronopathy link epilepsy and bipolar disorder.
Article in Molecular psychiatry, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.
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Who cites it
44 citing papers in PubMed, 103 citations in OpenAlex.
- Article
- Axon Initial Segment: Structure, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- A neuron type-specific microexon in Ank3/ankyrin-G modulates calcium activity and neuronal excitability.Nature communications · 2026Article
- Reframing the axon initial segment: Giant ankyrin-G as a modulator of excitability and plasticity in neurodevelopment.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- A neuron type-specific microexon inbioRxiv : the preprint server for biology · 2025Article
- A spatial long-read approach at near-single-cell resolution reveals developmental regulation of splicing and polyadenylation sites in distinct cortical layers and cell types.Nature communications · 2025Article
- Axon initial segment structure and function in health and disease.Physiological reviews · 2025Review
- Decoding Epilepsy: Prickle2 and Multifaceted Molecular Pathway Connections.Current pharmaceutical design · 2025Review
- Age-dependent regulation of axoglial interactions and behavior by oligodendrocyte AnkyrinG.Nature communications · 2024Article
- Voltage-gated sodium channels in genetic epilepsy: up and down of excitability.Journal of neurochemistry · 2024Review
- The Pathophysiological Underpinnings of Gamma-Band Alterations in Psychiatric Disorders.Life (Basel, Switzerland) · 2024Review
- Age-dependent regulation of axoglial interactions and behavior by oligodendrocyte AnkyrinG.bioRxiv : the preprint server for biology · 2024Article
- Abnormal patterns of sleep and waking behaviors are accompanied by neocortical oscillation disturbances in an Ank3 mouse model of epilepsy-bipolar disorder comorbidity.Translational psychiatry · 2023Article
- A characteristic cerebellar biosignature for bipolar disorder, identified with fully automatic machine learning.IBRO neuroscience reports · 2023Article
- Lithium rescues dendritic abnormalities in Ank3 deficiency models through the synergic effects of GSK3β and cyclic AMP signaling pathways.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023Article
- Homozygous Missense Variant in the N-Terminal Region of ANK3 Gene Is Associated with Developmental Delay, Seizures, Speech Abnormality, and Aggressive Behavior.Molecular syndromology · 2023Article
- DapBCH: a disease association prediction model Based on Cross-species and Heterogeneous graph embedding.Frontiers in genetics · 2023Article
- Palmitoylation controls the stability of 190 kDa ankyrin-G in dendritic spines and is regulated by ZDHHC8 and lithium.Frontiers in molecular neuroscience · 2023Article
- Animal models of Alzheimer's disease: Applications, evaluation, and perspectives.Zoological research · 2022Review
- Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
ANK3, encoding the adaptor protein Ankyrin-G (AnkG), has been implicated in bipolar disorder by genome-wide association studies. ANK3 has multiple alternative first exons, and a bipolar disorder-associated ANK3 variant has been shown to reduce the expression of exon 1b. Here we identify mechanisms through which reduced ANK3 exon 1b isoform expression disrupts neuronal excitation-inhibition balance. We find that parvalbumin (PV) interneurons and principal cells differentially express ANK3 first exon subtypes. PV interneurons express only isoforms containing exon 1b, whereas excitatory principal cells express exon 1e alone or both 1e and 1b. In transgenic mice deficient for exon 1b, PV interneurons lack voltage-gated sodium channels at their axonal initial segments and have increased firing thresholds and diminished action potential dynamic range. These mice exhibit an Ank3 gene dosage-dependent phenotype including behavior changes modeling bipolar disorder, epilepsy and sudden death. Thus ANK3's important association with human bipolar susceptibility may arise from imbalance between AnkG function in interneurons and principal cells and resultant excessive circuit sensitivity and output. AnkG isoform imbalance is a novel molecular endophenotype and potential therapeutic target.
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Registered trials
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