title: Divalent cation modulation of a-type potassium channels in acutely dissociated central neurons from wide-type and mutant Drosophila.
abstract: Drosophila mutants provide an ideal model to study channel-type specificity of ion channel regulation in situ. In this study, the effects of divalent cations on voltage-gated K+ currents were investigated in acutely dissociated central neurons of Drosophila third instar larvae using the whole-cell patch-clamp recording. Our data showed that micromolar Cd2+ enhanced the peak inactivating current (I(A)) without affecting the delayed component (I(K)). The same results were obtained in Ca(2+)-free external solution, and from slo1 mutation, which eliminates transient Ca(2+)-activated K+ current. Micromolar Cd2+ and Zn2+, and millimolar Ca2+ and Mg2+ all shifted the steady-state inactivation curve of I(A) without affecting the voltage-dependence of I(A) activation, whereas millimolar Cd2+ markedly affected both the activation and steady-state inactivation curves for I(A). Divalent cations affected I(A) with different potency; the sequence was: Zn2+ > Cd2+ > Ca2+ > Mg2+. The modulation of I(A) by Cd2+ was partially inhibited in Sh(M), a null Shaker (one of I(A)-encoding genes) mutation. Taken together, the channel-type specificity, the asymmetric effects on I(A) activation and inactivation kinetics, and the diverse potency of divalent cations all strongly support the idea that physiological divalent cations modulate A-type K+ channels through specific binding to extracellular sites of the channels.
authors: School of Life Sciences, University of Science and Technology of China, Hefei, China. tlxu@ion.ac.cn
authors: Tai-Xiang
authors: TX
authors: Xu
authors: Neng
authors: N
authors: Gong
authors: Tian-Le
authors: TL
authors: Xu
mesh_terms: D000818:Animals; D001921:Brain / Q000166:cytology* / Q000378:metabolism; D002104:Cadmium / Q000378:metabolism; D002118:Calcium / Q000378:metabolism; D002413:Cations, Divalent / Q000378:metabolism*; D029721:Drosophila Proteins / Q000235:genetics / Q000378:metabolism; D004331:Drosophila melanogaster / Q000235:genetics / Q000378:metabolism*; D051036:Large-Conductance Calcium-Activated Potassium Channels; D007814:Larva / Q000378:metabolism; D008274:Magnesium / Q000378:metabolism; D008564:Membrane Potentials / Q000502:physiology; D009154:Mutation; D009474:Neurons / Q000378:metabolism*; D015221:Potassium Channels / Q000235:genetics / Q000378:metabolism*; D024681:Potassium Channels, Calcium-Activated / Q000235:genetics / Q000378:metabolism; D051637:Shaker Superfamily of Potassium Channels; D015032:Zinc / Q000378:metabolism
chemical_list: D002413:Cations, Divalent; D029721:Drosophila Proteins; D051036:Large-Conductance Calcium-Activated Potassium Channels; D015221:Potassium Channels; D024681:Potassium Channels, Calcium-Activated; C496929:Sh protein, Drosophila; D051637:Shaker Superfamily of Potassium Channels; C494844:slo protein, Drosophila; D002104:Cadmium; D008274:Magnesium; D015032:Zinc; D002118:Calcium