title: Effects of prostaglandin F2α on small intestinal interstitial cells of Cajal.
abstract: OBJECTIVE
  To explore the role of prostaglandin F(2α) (PGF(2α))) on pacemaker activity in interstitial cells of Cajal (ICC) from mouse small intestine.
  
  
  METHODS
  In this study, effects of PGF(2α) in the cultured ICC cells were investigated with patch clamp technology combined with Ca(2+) image analysis.
  
  
  RESULTS
  Externally applied PGF(2α) (10 μmol/L) produced membrane depolarization in current-clamp mode and increased tonic inward pacemaker currents in voltage-clamp mode. The application of flufenamic acid (a non-selective cation channel inhibitor) or niflumic acid (a Cl(-) channel inhibitor) abolished the generation of pacemaker currents but only flufenamic acid inhibited the PGF(2α)-induced tonic inward currents. In addition, the tonic inward currents induced by PGF(2α) were not inhibited by intracellular application of 5'-[-thio]diphosphate trilithium salt. Pretreatment with Ca(2+) free solution, U-73122, an active phospholipase C inhibitor, and thapsigargin, a Ca(2+)-ATPase inhibitor in endoplasmic reticulum, abolished the generation of pacemaker currents and suppressed the PGF(2α)-induced tonic inward currents. However, chelerythrine or calphostin C, protein kinase C inhibitors, did not block the PGF(2α)-induced effects on pacemaker currents. When recording intracellular Ca(2+) ([Ca(2+)](i)) concentration using fluo-3/AM, PGF(2α) broadly increased the spontaneous [Ca(2+)](i) oscillations.
  
  
  CONCLUSIONS
  These results suggest that PGF(2α) can modulate pacemaker activity of ICC by acting non-selective action channels through phospholipase C-dependent pathway via [Ca(2+)]i regulation.
authors: Department of Internal Medicine, College of Medicine, Chosun University, Gwangju 501-759, South Korea.
authors: Chan Guk
authors: CG
authors: Park
authors: Young Dae
authors: YD
authors: Kim
authors: Man Yoo
authors: MY
authors: Kim
authors: Jae Woong
authors: JW
authors: Koh
authors: Jae Yeoul
authors: JY
authors: Jun
authors: Cheol Ho
authors: CH
authors: Yeum
authors: Insuk
authors: I
authors: So
authors: Seok
authors: S
authors: Choi
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology; D001683:Biological Clocks / Q000187:drug effects / Q000502:physiology; D002118:Calcium / Q000378:metabolism; D002478:Cells, Cultured; D015237:Dinoprost / Q000494:pharmacology*; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005439:Flufenamic Acid / Q000494:pharmacology; D056885:Interstitial Cells of Cajal / Q000166:cytology / Q000187:drug effects*; D007421:Intestine, Small / Q000166:cytology*; D007473:Ion Channels / Q000378:metabolism; D008564:Membrane Potentials / Q000502:physiology; D051379:Mice; D008807:Mice, Inbred BALB C; D009544:Niflumic Acid / Q000494:pharmacology; D018408:Patch-Clamp Techniques; D010738:Type C Phospholipases / Q000037:antagonists & inhibitors / Q000378:metabolism
chemical_list: D000893:Anti-Inflammatory Agents; D004791:Enzyme Inhibitors; D007473:Ion Channels; D009544:Niflumic Acid; D005439:Flufenamic Acid; D015237:Dinoprost; D010738:Type C Phospholipases; D002118:Calcium