title: Muscle and motor-skill dysfunction in a K+ channel-deficient mouse are not due to altered muscle excitability or fiber type but depend on the genetic background.
abstract: The voltage-gated K+ channel Kv3.1 is expressed in skeletal muscle and in GABAergic interneurons in the central nervous system. Hence, the absence of Kv3.1 K+ channels may lead to a phenotype of myogenic or neurogenic origin, or both. Kv3.1-deficient (Kv3.1-/-) 129/Sv mice display altered contractile properties of their skeletal muscles and show poor performance on a rotating rod. In contrast, Kv3.1-/- mice on the (129/Sv x C57BL/6)F1 background display normal muscle properties and perform like wild-type mice. The correlation of poor performance on the rotating rod with altered muscle properties supports the notion that the skeletal muscle dysfunction in Kv3.1-/- 129/Sv mice may be responsible for the impaired motor skills on the rotating rod. Surprisingly, we did not find major differences between wild-type and Kv3.1-/- 129/Sv skeletal muscles in either the resting or action potential, the delayed-rectifier potassium conductance (gK) or the distribution of fast and slow muscle fibers. These findings suggest that the Kv3.1 K+ channel may not play a major role in the intrinsic excitability of skeletal muscle fibers although its absence leads to slower contraction and relaxation and to smaller forces in muscles of 129/Sv Kv3.1-/- mice.
authors.affiliation: Department of Pharmacology, Mexico DF, Mexico.
authors.forename: J A
authors.initials: JA
authors.lastname: Sánchez
authors.forename: C S
authors.initials: CS
authors.lastname: Ho
authors.forename: D M
authors.initials: DM
authors.lastname: Vaughan
authors.forename: M C
authors.initials: MC
authors.lastname: Garcia
authors.forename: R W
authors.initials: RW
authors.lastname: Grange
authors.forename: R H
authors.initials: RH
authors.lastname: Joho
mesh_terms: D000200:Action Potentials / Q000235:genetics; D000818:Animals; D051668:Delayed Rectifier Potassium Channels; D005260:Female; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D018345:Mice, Knockout; D019957:Motor Skills Disorders / Q000201:enzymology / Q000235:genetics*; D009119:Muscle Contraction / Q000235:genetics* / Q000502:physiology; D018485:Muscle Fibers, Skeletal / Q000201:enzymology*; D018482:Muscle, Skeletal / Q000201:enzymology; D009135:Muscular Diseases / Q000201:enzymology / Q000235:genetics*; D009218:Myosins / Q000378:metabolism; D009479:Neuropeptides / Q000172:deficiency* / Q000235:genetics; D011188:Potassium / Q000378:metabolism; D015221:Potassium Channels / Q000172:deficiency* / Q000235:genetics / Q000378:metabolism; D024642:Potassium Channels, Voltage-Gated; D051670:Shaw Potassium Channels
chemical_list: D051668:Delayed Rectifier Potassium Channels; D009479:Neuropeptides; D015221:Potassium Channels; D024642:Potassium Channels, Voltage-Gated; D051670:Shaw Potassium Channels; D009218:Myosins; D011188:Potassium