Abstract
Acute stimulation of protein kinase C (PKC) inhibited glucose‐induced slow oscillations in cytoplasmic free Ca2+‐concentration, [Ca2+]i, in mouse pancreatic B‐cells. In PKC‐depleted cells glucose induced rapid transients in [Ca2+]i, lasting for approximately 10 s, superimposed on the slow oscillations in [Ca2+]i. It was demonstrated that the transients did not occur in the absence of extracellular Ca2+. Each transient typically was preceded by a slow increase in [Ca2+]i, representing the rising phase of an ordinary glucose‐induced slow oscillation, and the [Ca2+]i, immediately after a transient was lower than just before the spike. These data further emphasize the interplay between voltage‐dependent Ca2+‐channels and the phospholipase C system in the regulation of B‐cell [Ca2+]i‐oscillations.
