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• W1540396301 endingPage "171" @default.
• W1540396301 startingPage "159" @default.
• W1540396301 abstract "Zinc (Zn 2+ ) functions as a signalling molecule in the nervous system and modulates many ionic channels. In this study, we have explored the effects of Zn 2+ on recombinant T‐type calcium channels (Ca V 3.1, Ca V 3.2 and Ca V 3.3). Using tsA‐201 cells, we demonstrate that Ca V 3.2 current (IC 50 , 0.8 μ m ) is significantly more sensitive to Zn 2+ than are Ca V 3.1 and Ca V 3.3 currents (IC 50 , 80 μ m and ∼160 μ m , respectively). This inhibition of Ca V 3 currents is associated with a shift to more negative membrane potentials of both steady‐state inactivation for Ca V 3.1, Ca V 3.2 and Ca V 3.3 and steady‐state activation for Ca V 3.1 and Ca V 3.3 currents. We also document changes in kinetics, especially a significant slowing of the inactivation kinetics for Ca V 3.1 and Ca V 3.3, but not for Ca V 3.2 currents. Notably, deactivation kinetics are significantly slowed for Ca V 3.3 current (∼100‐fold), but not for Ca V 3.1 and Ca V 3.2 currents. Consequently, application of Zn 2+ results in a significant increase in Ca V 3.3 current in action potential clamp experiments, while Ca V 3.1 and Ca V 3.2 currents are significantly reduced. In neuroblastoma NG 108‐15 cells, the duration of Ca V 3.3‐mediated action potentials is increased upon Zn 2+ application, indicating further that Zn 2+ behaves as a Ca V 3.3 channel opener. These results demonstrate that Zn 2+ exhibits differential modulatory effects on T‐type calcium channels, which may partly explain the complex features of Zn 2+ modulation of the neuronal excitability in normal and disease states." @default.
• W1540396301 created "2016-06-24" @default.
• W1540396301 creator A5035869933 @default.
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• W1540396301 creator A5046389822 @default.
• W1540396301 creator A5048169572 @default.
• W1540396301 creator A5061728673 @default.
• W1540396301 date "2006-12-21" @default.
• W1540396301 modified "2023-10-15" @default.
• W1540396301 title "Subunit-specific modulation of T-type calcium channels by zinc" @default.
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• W1540396301 doi "https://doi.org/10.1113/jphysiol.2006.114496" @default.
• W1540396301 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2075129" @default.
• W1540396301 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/17082234" @default.
• W1540396301 hasPublicationYear "2006" @default.
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