Role of BK potassium channels shaping action potentials and the associated [Ca(2+)](i) oscillations in GH(3) rat anterior pituitary cells.

Abstract

Measurements of electrical activity and intracellular Ca(2+) levels were performed in perforated-patch clamped GH(3) cells to determine the contribution of large-conductance calcium-activated K(+) (BK) channels to action potential repolarization and size of the associated Ca(2+) oscillations. By examining the dependence of action potential (AP) duration on extracellular Ca(2+) levels in the presence and the absence of the specific BK channel blocker paxilline, it is observed that plateau-like action potentials are associated to low densities of paxilline-sensitive currents. Extracellular Ca(2+) increases or paxilline additions are not able to largely modify action potential duration in cells showing a reduced expression of BK currents. Furthermore, specific blockade of these currents with paxilline systematically elongates AP duration, but only under conditions in which short APs and/or prominent BK currents recorded under voltage-clamp mode are present in the same cells. Our data indicate that in GH(3) cells, BK channels act primarily ending the action potential and suggest that by contributing to fine-tuning cellular electrical properties and hence intracellular Ca(2+) variations, BK channels may play an important role on time- and cell-dependent modulation of physiological outputs in adenohypophyseal cells.