ArticlePflugers Archiv : European journal of physiology1994
Differential modulation of pharmacologically distinct components of Ca2+ currents by protein kinase C activators and phosphatase inhibitors in nerve-growth-factor-differentiated rat pheochromocytoma (PC12) cells.
Article in Pflugers Archiv : European journal of physiology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed, 13 citations in OpenAlex.
- Mechanism of dopamine mediated inhibition of neuropeptide Y release from pheochromocytoma cells (PC12 cells).Biochemical pharmacology · 2007Article
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2 authors at 1 institution in 1 country.
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Abstract
We have studied the effects of protein kinase C (PKC) activators 4 beta-phorbol 12-myristate 13-acetate (4 beta-PMA) and 1-oleoyl-2-acetylglycerol (OAG) and of phosphatase inhibitors (okadaic acid and calyculin A) on voltage-activated Ca2+ and K+ channels in nerve-growth-factor-(NGF)-differentiated pheochromocytoma (PC12) cells. Whole-cell Ba2+ and K+ currents were recorded at room temperature with the patch-clamp technique. By using omega-conotoxin (CgTX) and isradipine, two specific Ca2+ channel blockers, we found three types of Ba2+ currents (IBa): (1) a omega-CgTX-sensitive IBa; (2) an isradipine-sensitive IBa; and (3) a omega-CgTX plus isradipine-resistant IBa. The external application of 4 beta-PMA or OAG down-modulated the isradipine-sensitive IBa whereas the two other IBa were not affected. 4 beta-PMA-induced inhibition of IBa was prevented by staurosporine (a protein kinase inhibitor) and PKC (19-31) (a specific PKC inhibitor). The delayed rectifier K+ current (IK) was unaffected by PKC activators. Both okadaic acid and calyculin A affected the components of the IBa in different manners. The presence of okadaic acid decreased the isradipine-sensitive IBa more than the omega-CgTX-sensitive IBa. The omega-CgTX plus isradipine-resistant IBa was not affected. Calyculin A down-modulated all three components of IBa to a similar degree. Our results suggest a differential modulation of voltage-activated Ca2+ and K+ channels by the PKC signalling pathway in NGF-differentiated PC12 cells.
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