Electrophysiological Properties of Gastric Pacemaker Potentials(PACEMAKER CELLS IN THE HEART AND GUT)

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Electrophysiological properties of pacemaker potentials recorded from myenteric interstitial cells of Cajal (ICC-MY) within the guinea-pig gastric antrum are reviewed briefly. Pacemaker potentials consist of two components, a primary component forming a transient depolarization with a rapidly rising initial phase, followed by a secondary component as a plateau with sustained depolarization. The primary component is inhibited by low [Ca^<2+>]_0 solutions or depolarization of the membrane with high [K^+]_0 solutions. This inhibition could be mimicked by chelating [Ca^<2+>]_1 with BAPTA-AM, suggesting that this component is produced by activation of voltage-dependent Ca^<2+> permeable channels. The plateau component is inhibited by low [Cl^-]_0 solution or DIDS, an inhibitor of Ca^<2+>-activated Cl^--channels, suggesting that this component is formed by Ca^<2+>-activated Cl^--currents. Reduction of Ca^<2+> release from internal stores by inhibiting the internal Ca-pump with cyclopiazonic acid results in a shortened duration of the plateau component, with no alteration in the rate of rise of the primary component. 2-APB, an inhibitor of the IP_3-receptor mediated Ca^<2+> release from internal stores, abolishes pacemaker potentials, suggesting that the release of Ca^<2+> from internal IP_3-sensitive Ca^<2+> stores is required for generation of pacemaker potentials. CCCP, a mitochondrial protonophore, depolarizes the membrane and abolishes pacemaker potentials, suggesting that mitochondrial Ca^<2+> handling functions may be coupled with generation of pacemaker potentials. These results indicate that the two components of pacemaker potentials are generated by different mechanisms; the primary component may be produced by activation of voltage-dependent Ca^<2+>-permeable channels, while the plateau component may be produced by the opening of Ca^<2+>-activated Cl^--channels. It is hypothesized that pacemaker potentials are initiated by depolarization of the membrane due to generation of unitary potentials in response to mitochondrial Ca^<2+> handling. Activation of voltage-dependent Ca^<2+> influx, IP_3-receptor mediated Ca^<2+> release from the internal stores and Ca^<2+>-activated Cl^--channels may be involved as successive steps downstream to the generation of unitary potentials.
日本平滑筋学会の論文

Electrophysiological Properties of Gastric Pacemaker Potentials(PACEMAKER CELLS IN THE HEART AND GUT)

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