FUNCTIONAL EXPRESSION OF SHAKER K-NEURONS DERIVED FROM SH CDNA TRANSFORMANTS - DISTINCT PROPERTIES, DISTRIBUTION, AND TURNOVER( CHANNELS INCULTURED DROSOPHILA GIANT)

Citation
Ml. Zhao et al., FUNCTIONAL EXPRESSION OF SHAKER K-NEURONS DERIVED FROM SH CDNA TRANSFORMANTS - DISTINCT PROPERTIES, DISTRIBUTION, AND TURNOVER( CHANNELS INCULTURED DROSOPHILA GIANT), The Journal of neuroscience, 15(2), 1995, pp. 1406-1418
Citations number
57
Categorie Soggetti
Neurosciences,Neurosciences
Journal title
ISSN journal
02706474
Volume
15
Issue
2
Year of publication
1995
Pages
1406 - 1418
Database
ISI
SICI code
0270-6474(1995)15:2<1406:FEOSKD>2.0.ZU;2-X
Abstract
Expression of transgenic Shaker (Sh) channels has not previously been examined in Drosophila neurons. We studied K+ current by whole-cell re cording in cultured ''giant'' neurons derived from germline transforma nts. Independent lines were generated by using a P-element vector, in which transcription of the 29-4 cDNA, one of the Sh splicing variants (Iverson and Rudy, 1990), was under the control of a heat shock (HS)-i nducible promoter. Transformants in wildtype and two different Sh muta nt backgrounds all exhibited an HS-inducible, A-type K+ current that w as characterized by a much slower recovery from inactivation and a hig her sensitivity to 4-aminopyridine than native K+ currents or Sh 29-4 currents expressed in Xenopus oocytes. Despite similarities in the kin etic and pharmacological properties of the HS-induced current in all b ackgrounds examined, host-dependent differences in the peak current am plitude have been consistently observed between multiple lines of 29-4 Sh(M) and 29-4 Sh(120) that might reflect differential channel subuni t assembly in different hosts. Isolation of the novel 29-4 currents al lowed determination of the channel turnover rate in cultured neurons. These currents persisted for up to 3 d or more, comparable with the du rations previously reported for Na+ and Ca2+ channels. Surprisingly, t he percentage of cells expressing inactivating K+ currents remained ap proximately the same with or without HS induction, suggesting that som e mechanisms exist to restrict functional expression of inactivating K + channels, including transgenic Sh channels and those trot encoded by the Sh locus, to certain types of neurons.