“…A number of possible mechanisms have been considered, including allosteric regulation of Ca2+ channel function (Plant, Standen & Ward, 1983), modulation of voltage-dependent inactivation by Ca2+ (Lee, Marban & Tsien, 1985), and activation of Ca2+-dependent phosphatases (Chad & Eckert, 1986). While this last hypothesis is supported by repeated suggestions that only phosphorylated Ca2+ channels are functional (Sperelakis & Schneider, 1976;Reuter & Scholz, 1977;Bean, Nowycky & Tsien, 1984; Armstrong & Eckert, 1987;Hymel, Striessnig, Glossmann & Schindler, 1988; Nunoki, Florio & Catterall, 1989), an absolute requirement for channel phosphorylation has been disputed vigorously (Kameyama, Hescheler, Hofmann Kameyama, Hescheler, Mieskes & Trautwein, 1986;Trautwein, Cavalie, Flockerzi, Hofmann & Pelzer, 1987). Furthermore, even if this point were conceded it would still leave open the question of whether a rise in [Ca2+]i promotes Ca2+ channel dephosphorylation (Byerly, Leung & Yazejian, 1988 (Hadiey & Lederer, 1991 a).…”