ArticlePhysiological reports2016
The contribution of Kv2.2-mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons.
Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- A Kv2 inhibitor combination reveals native neuronal conductances consistent with Kv2/KvS heteromers.eLife · 2025Article
- Mono-allelic KCNB2 variants lead to a neurodevelopmental syndrome caused by altered channel inactivation.American journal of human genetics · 2024Article
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KThe Journal of comparative neurology · 2024Article
- Distinct cellular expression and subcellular localization of Kv2 voltage-gated KbioRxiv : the preprint server for biology · 2023Article
- Multitarget nociceptor sensitization by a promiscuous peptide from the venom of the King Baboon spider.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- The role of voltage-gated ion channels in visual function and disease in mammalian photoreceptors.Pflugers Archiv : European journal of physiology · 2021Review
- SP6616 as a Kv2.1 inhibitor efficiently ameliorates peripheral neuropathy in diabetic mice.EBioMedicine · 2020Article
- The contribution of Kv2.2-mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons.Physiological reports · 2016Article
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5 authors.
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Abstract
Delayed rectifier voltage-gated K(+)(Kv) channels play an important role in the regulation of the electrophysiological properties of neurons. In mouse dorsal root ganglion (DRG) neurons, a large fraction of the delayed rectifier current is carried by both homotetrameric Kv2 channels and heterotetrameric channels consisting of Kv2 and silent Kv (KvS) subunits (i.e., Kv5-Kv6 and Kv8-Kv9). However, little is known about the contribution of Kv2-mediated currents during the postnatal development ofDRGneurons. Here, we report that the Stromatoxin-1 (ScTx)-sensitive fraction of the total outward K(+)current (IK) from mouseDRGneurons gradually decreased (~13%,P < 0.05) during the first month of postnatal development. Because ScTx inhibits both Kv2.1- and Kv2.2-mediated currents, this gradual decrease may reflect a decrease in currents containing either subunit. However, the fraction of Kv2.1 antibody-sensitive current that only reflects the Kv2.1-mediated currents remained constant during that same period. These results suggested that the fractional contribution of Kv2.2-mediated currents relative toIKdecreased with postnatal age. SemiquantitativeRT-PCRanalysis indicated that this decrease can be attributed to developmental changes in Kv2.2 expression as themRNAlevels of the Kv2.2 subunit decreased gradually between 1 and 4 weeks of age. In addition, we observed age-dependent fluctuations in themRNAlevels of the Kv6.3, Kv8.1, Kv9.1, and Kv9.3 subunits. These results support an important role of both Kv2 and KvS subunits in the postnatal maturation ofDRGneurons.
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