ArticleStem cell research2013
BDNF profoundly and specifically increases KCNQ4 expression in neurons derived from embryonic stem cells.
Article in Stem cell research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 18 citations in OpenAlex.
- Differentiation and characterization of neurons derived from rat iPSCs.Journal of neuroscience methods · 2020Article
- Kv7 channels are upregulated during striatal neuron development and promote maturation of human iPSC-derived neurons.Pflugers Archiv : European journal of physiology · 2018Article
- Ultracompact Microwatt CMOS Current Readout With Picoampere Noise and Kilohertz Bandwidth for Biosensor Arrays.IEEE transactions on biomedical circuits and systems · 2018Article
- Firing frequency and entrainment maintained in primary auditory neurons in the presence of combined BDNF and NT3.Scientific reports · 2016Article
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Neurons resembling the spiral ganglion neurons (SGNs) of the auditory nerve can be generated from embryonic stem cells through induced overexpression of the transcription factor Neurogenin-1 (Neurog1). While recapitulating this developmental pathway produces glutamatergic, bipolar neurons reminiscent of SGNs, these neurons are functionally immature, being characterized by a depolarized resting potential and limited excitability. We explored the effects of two neurotrophins known to be present in the inner ear, brain derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3), on the electrophysiology of neurons following Neurog1 induction. Our data reveal a significant reduction in resting membrane potential (RMP) following neurotrophin exposure, with BDNF producing a more robust effect than NT-3. This effect was accompanied by a profound and specific upregulation of the KCNQ4 subtype, where a 9-fold increase was observed with quantitative PCR. The other neuronally expressed KCNQ subtypes (2, 3, and 5) exhibited upregulation which was 3-fold or less in magnitude. Quantitative immunohistochemistry confirmed the increase in KCNQ4 expression at the protein level. The present data show a novel link between BDNF and KCNQ4 expression, yielding insight into the restricted expression pattern of a channel known to play special roles in setting the resting potential of auditory cells and in the etiology of progressive high-frequency hearing loss.
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