title: The contribution of Kv2.2-mediated currents decreases during the postnatal development of mouse dorsal root ganglion neurons.
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.
authors.affiliation: Laboratory for Molecular Biophysics, Physiology and Pharmacology, Department of Biomedical Sciences, University of Antwerp, CDE, Antwerpen, Belgium.
authors.forename: Glenn
authors.initials: G
authors.lastname: Regnier
authors.affiliation: Laboratory for Molecular Biophysics, Physiology and Pharmacology, Department of Biomedical Sciences, University of Antwerp, CDE, Antwerpen, Belgium.
authors.forename: Elke
authors.initials: E
authors.lastname: Bocksteins
authors.affiliation: Laboratory for Cardiovascular Research, Institute Born-Bunge University of Antwerp, CDE, Antwerpen, Belgium.
authors.forename: Gerda
authors.initials: G
authors.lastname: Van de Vijver
authors.affiliation: Laboratory for Molecular Biophysics, Physiology and Pharmacology, Department of Biomedical Sciences, University of Antwerp, CDE, Antwerpen, Belgium dirk.snyders@uantwerpen.be.
authors.forename: Dirk J
authors.initials: DJ
authors.lastname: Snyders
authors.affiliation: Laboratory for Cardiovascular Research, Institute Born-Bunge University of Antwerp, CDE, Antwerpen, Belgium.
authors.forename: Pierre-Paul
authors.initials: PP
authors.lastname: van Bogaert
mesh_terms: D000367:Age Factors; D000818:Animals; D005727:Ganglia, Spinal / Q000187:drug effects / Q000254:growth & development / Q000378:metabolism*; D018507:Gene Expression Regulation, Developmental; D015640:Ion Channel Gating; D008297:Male; D008564:Membrane Potentials; D008810:Mice, Inbred C57BL; D009474:Neurons / Q000187:drug effects / Q000378:metabolism*; D010455:Peptides / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D026902:Potassium Channel Blockers / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D051669:Shab Potassium Channels / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D013111:Spider Venoms / Q000494:pharmacology
chemical_list: C496990:Kcnb1 protein, mouse; C496993:Kcnb2 protein, mouse; D010455:Peptides; D026902:Potassium Channel Blockers; D012333:RNA, Messenger; D051669:Shab Potassium Channels; D013111:Spider Venoms; C560803:stromatoxin protein, Stromatopelma calceata; D011188:Potassium
keywords: Dorsal root ganglion neurons; Kv2; Kv5‐Kv9; postnatal development