ArticleThe Journal of physiology2012
Kv1.1-dependent control of hippocampal neuron number as revealed by mosaic analysis with double markers.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Loss of functional System x-c uncouples aberrant postnatal neurogenesis from epileptogenesis in the hippocampus of Kcna1-KO mice.Cell reports · 2022Article
- KProceedings of the National Academy of Sciences of the United States of America · 2022Article
- Article
- Kv1.1 channels regulate early postnatal neurogenesis in mouse hippocampus via the TrkB signaling pathway.eLife · 2021Article
- Article
- Linking neuronal lineage and wiring specificity.Neural development · 2018Review
- Precision physiology and rescue of brain ion channel disorders.The Journal of general physiology · 2017Review
- Tau loss attenuates neuronal network hyperexcitability in mouse and Drosophila genetic models of epilepsy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Article
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Authors and funding
6 authors.
Funding
Abstract
Megencephaly, or mceph, is a spontaneous frame-shift mutation of the mouse Kv1.1 gene. This mceph mutation results in a truncated Kv1.1 channel α-subunit without the channel pore domain or the voltage sensor. Interestingly, mceph/mceph mouse brains are enlarged and – unlike wild-type mouse brains – they keep growing throughout adulthood, especially in the hippocampus and ventral cortex. We used mosaic analysis with double markers (MADM) to identify the underlying mechanism. In mceph-MADM6 mice with only a small fraction of neurons homozygous for the mceph mutation, those homozygous mceph/mceph neurons in the hippocampus are more abundant than wild-type neurons produced by sister neural progenitors. In contrast, neither mceph/mceph astrocytes, nor neurons in the adjacent dorsal cortex (including the entorhinal and parietal cortex) exhibited overgrowth in the adult brain. The sizes of mceph/mceph hippocampal neurons were comparable to mceph/+ or wild-type neurons. Our mosaic analysis reveals that loss of Kv1.1 function causes an overproduction of hippocampal neurons, leading to an enlarged brain phenotype.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.