ArticleProceedings of the National Academy of Sciences of the United States of America2021
Developmental HCN channelopathy results in decreased neural progenitor proliferation and microcephaly in mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Shared Disease Mechanisms in Neurodevelopmental Disorders: A Cellular and Molecular Biology Perspective.Brain sciences · 2025Review
- A comprehensive review of HCN channel expression and IJournal of neurophysiology · 2025Review
- Role of HCN channels in the functions of basal ganglia and Parkinson's disease.Cellular and molecular life sciences : CMLS · 2024Review
- Downregulation of CDC25C in NPCs Disturbed Cortical Neurogenesis.International journal of molecular sciences · 2023Article
- Seizures, behavioral deficits, and adverse drug responses in two new genetic mouse models ofeLife · 2022Article
- A matter of space and time: Emerging roles of disease-associated proteins in neural development.Neuron · 2022Review
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The development of the cerebral cortex relies on the controlled division of neural stem and progenitor cells. The requirement for precise spatiotemporal control of proliferation and cell fate places a high demand on the cell division machinery, and defective cell division can cause microcephaly and other brain malformations. Cell-extrinsic and -intrinsic factors govern the capacity of cortical progenitors to produce large numbers of neurons and glia within a short developmental time window. In particular, ion channels shape the intrinsic biophysical properties of precursor cells and neurons and control their membrane potential throughout the cell cycle. We found that hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channel subunits are expressed in mouse, rat, and human neural progenitors. Loss of HCN channel function in rat neural stem cells impaired their proliferation by affecting the cell-cycle progression, causing G1 accumulation and dysregulation of genes associated with human microcephaly. Transgene-mediated, dominant-negative loss of HCN channel function in the embryonic mouse telencephalon resulted in pronounced microcephaly. Together, our findings suggest a role for HCN channel subunits as a part of a general mechanism influencing cortical development in mammals.
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