title: Disruption of actin cytoskeleton in cultured rat astrocytes suppresses ATP- and bradykinin-induced [Ca(2+)](i) oscillations by reducing the coupling efficiency between Ca(2+) release, capacitative Ca(2+) entry, and store refilling.
abstract: Oscillations of [Ca(2+)](i) which are believed to be important in regulation of cellular behaviour or gene expression, require Ca(2+) entry via capacitative Ca(2+) influx for store refilling. However, the mediator between Ca(2+) store content and activation of Ca(2+) influx is still elusive. There is also controversy about the role of the actin cytoskeleton in this coupling. Therefore, the importance of an intact actin cytoskeleton on ATP- and bradykinin-elicited Ca(2+) signalling was investigated in cultured rat astrocytes by treatment with cytochalasin D which changes the morphology of the cells from an extended to a rounded shape. Cytochalasin D-treated astrocytes were unable, upon prolonged stimulation with the P2Y receptor agonist ATP, to generate oscillations of [Ca(2+)](i) which are, however, seen in 54% of untreated control cells. In cytochalasin D-treated cells, the amplitude of the initial Ca(2+) response was reduced mainly by disturbing the Ca(2+) influx, and, moreover, the total Ca(2+) pool which is sensitive to thapsigargin or cyclopiazonic acid was diminished.Thus, disruption of the cytoskeleton blocks agonist-elicited [Ca(2+)](i) oscillations apparently by reducing the coupling efficiency between intracellular Ca(2+) stores and capacitative Ca(2+) entry.
authors.affiliation: Institut für Neurobiochemie, Otto-von-Guericke-Universität Magdeburg, Medizinische Fakultät, Leipziger Strasse 44, 39120, Magdeburg, Germany.
authors.forename: M
authors.initials: M
authors.lastname: Sergeeva
authors.forename: J J
authors.initials: JJ
authors.lastname: Ubl
authors.forename: G
authors.initials: G
authors.lastname: Reiser
mesh_terms: D000199:Actins / Q000187:drug effects / Q000502:physiology*; D000255:Adenosine Triphosphate / Q000494:pharmacology*; D000818:Animals; D001253:Astrocytes / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D001692:Biological Transport; D001920:Bradykinin / Q000494:pharmacology*; D001921:Brain / Q000166:cytology / Q000502:physiology; D002118:Calcium / Q000378:metabolism*; D020013:Calcium Signaling / Q000187:drug effects / Q000502:physiology; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D002478:Cells, Cultured; D015638:Cytochalasin D / Q000494:pharmacology; D003599:Cytoskeleton / Q000502:physiology*; D007211:Indoles / Q000494:pharmacology; D007700:Kinetics; D051381:Rats; D018048:Receptors, Purinergic P2 / Q000502:physiology
chemical_list: D000199:Actins; D007211:Indoles; D018048:Receptors, Purinergic P2; D015638:Cytochalasin D; D000255:Adenosine Triphosphate; D000252:Calcium-Transporting ATPases; D001920:Bradykinin; D002118:Calcium; C000543:cyclopiazonic acid