Electrophysiological properties of gastric pacemaker potentials.
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 [Ca2+]o solutions or depolarization of the membrane with high [K+]o solutions. This inhibition could be mimicked by chelating [Ca2+]i with BAPTA-AM, suggesting that this component is produced by activation of voltage-dependent Ca2+ permeable channels. The plateau component is inhibited by low [Cl-]o solution or DIDS, an inhibitor of Ca2+-activated Cl(-)-channels, suggesting that this component is formed by Ca2+-activated Cl(-)-currents. Reduction of Ca2+ 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 IP3-receptor mediated Ca2+ release from internal stores, abolishes pacemaker potentials, suggesting that the release of Ca2+ from internal IP3-sensitive Ca2+ stores is required for generation of pacemaker potentials. CCCP, a mitochondrial protonophore, depolarizes the membrane and abolishes pacemaker potentials, suggesting that mitochondrial Ca2+ 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 Ca2+-permeable channels, while the plateau component may be produced by the opening of Ca2+-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 Ca2+ handling. Activation of voltage-dependent Ca2+ influx, IP3-receptor mediated Ca2+ release from the internal stores and Ca2+-activated Cl(-)-channels may be involved as successive steps downstream to the generation of unitary potentials.
Kito
Yoshihiko
Y
Department of Physiology, Nagoya City University Medical School, Mizuho-ku, Nagoya 467-8601, Japan.
Suzuki
Hikaru
H
D000818:Animals; D001683:Biological Clocks / Q000502:physiology*; D004594:Electrophysiology; D006801:Humans; D013270:Stomach / Q000166:cytology* / Q000502:physiology* / Q000503:physiopathology; D013272:Stomach Diseases / Q000503:physiopathology