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Am J Physiol Gastrointest Liver Physiol 275: G550-G555, 1998;
0193-1857/98 $5.00
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Vol. 275, Issue 3, G550-G555, September 1998

Capacitative Ca2+ entry in enteric glia induced by thapsigargin and extracellular ATP

George A. Sarosi, Douglas C. Barnhart, Douglas J. Turner, and Michael W. Mulholland

Department of Surgery, University of Michigan, Ann Arbor, Michigan 48109-0331

Mobilization of intracellular Ca2+ stores is coupled to Ca2+ influx across the plasma membrane, a process termed capacitative Ca2+ entry. Capacitative Ca2+ entry was examined in cultured guinea pig enteric glia exposed to 100 µM ATP, an inositol trisphosphate-mediated Ca2+-mobilizing agonist, and to 1 µM thapsigargin, an inhibitor of microsomal Ca2+ ATPase. Both agents caused mobilization of intracellular Ca2+ stores followed by influx of extracellular Ca2+. This capacitative Ca2+ influx was inhibited by Ni2+ (88 ± 1%) and by La3+ (87 ± 1%) but was not affected by L- or N-type Ca2+ channel blockers. Pretreatment of glia with 100 nM phorbol 12-myristate 13-acetate for 24 h decreased capacitative Ca2+ entry by 48 ± 2%. Chelerythrine (0.1-10 µM), a specific antagonist of protein kinase C (PKC), dose dependently inhibited capacitative Ca2+ entry. The nitric oxide synthase inhibitor NG-nitro-L-arginine (1 mM) decreased Ca2+ influx by 42 ± 1%. Capacitative Ca2+ entry was inhibited to a similar degree by the guanylate cyclase inhibitor (1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one). Capacitative Ca2+ entry occurs in enteric glial cells via lanthanum-inhibitable channels through a process regulated by PKC and nitric oxide.

glial cell; endothelin; myenteric plexus


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