Journal
FEBS LETTERS
Volume 473, Issue 2, Pages 265-268Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/S0014-5793(00)01532-5
Keywords
protein kinase inhibitor; protein kinase C; glutamate release; Na+ channel; synaptosome; dorsal root ganglion neuron
Funding
- NIGMS NIH HHS [GM 58055] Funding Source: Medline
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We find that several protein kinase C (PKC) inhibitors, previously considered to be specific, directly inhibit voltage-dependent Na+ channels at their useful concentrations. Bisindolylmaleimide I (GF 1092037), IX (Ro 31-8220) and V (an inactive analogue), but not H7 (a non-selective isoquinolinesulfonamide protein kinase inhibitor), inhibited Na+ channels assessed by several independent criteria: Na+ channel-dependent glutamate release and [H-3]batrachotoxinin-A 20-alpha-benzoate binding in rat cortical synaptosomes, veratridine-stimulated Na-22(+) influx in CHO cells expressing rat CNaIIa Na+ channels and Na+ currents measured in isolated rat dorsal root ganglion neurons by whole cell patch-clamp recording. These findings limit the usefulness of the bisindolylmaleimide class PKC inhibitors in excitable cells. (C) 2000 Federation of European Biochemical Societies.
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