Exposure of non-excitatory cells to the tyrosine kinase (PTK) inhibitors, genistein, herbimycin A, and tyrphostin, induced at least two families of K f currents. The first, a TEA-insensitive slow-inactivating K + current, is induced within 3 min following treatment with 140 m M genistein or 100 n M
Modulation of rat skeletal muscle chloride channels by activators and inhibitors of protein kinase C
β Scribed by D. Tricarico; D. Conte Camerino; S. Govoni; S. H. Bryant
- Book ID
- 104787223
- Publisher
- Springer
- Year
- 1991
- Tongue
- English
- Weight
- 451 KB
- Volume
- 418
- Category
- Article
- ISSN
- 0031-6768
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β¦ Synopsis
The membrane electrical parameters and component conductances of rat extensor digitorum longus muscle fibres were studied in vitro at 30 ~ with standard two microelectrode square pulse cable analysis in the presence of protein kinase C (PKC) activators and inhibitors. The PKC activator, 4-[3-phorbol-12,13 dibutyrate (4-13-PDB), (2-90 nM) blocked up to 67% chloride conductance (Gcl) in rat skeletal muscle fibres and induced myotonic hyperexcitability. The concentration necessary to produce a 50% block of the membrane Gcl was 23 nM. The "inactive" 4-a-phorbol-12,13 dibutyrate had no effect at 2 gM. The blocking effect of 4-13-PDB on Gcl was prevented by preincubation of the preparations with the PKC inhibitors, staurosporine (1-5 ~tM) and tetrahydropapaverolone (50-100 txM). The blocking effects on membrane Gcl of 4-13-PDB and its antagonism by the inhibitors used support the concept of the involvement of PKC in regulating C1 channels of mammalian skeletal muscle fibres.
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