ROLE OF LOCAL CA-2-2+-INDUCED CA-2+ RELEASE IN CRAYFISH MUSCLE-FIBERS( DOMAINS IN ACTIVATION OF CA)

Simultaneous measurements were made of crayfish muscle Ca2+ currents ( I(Ca)) and the intracellular Ca2+ transients they elicit due to Ca2+-i nduced Ca2+ release (CICR) from the sarcoplasmic reticulum (SR). Ca2concentration ([Ca2+]) elevations produced by Ca2+ entry via I(Ca) wer e much more effective in triggering CICR than were ongoing release or homogeneous elevations of Ca2+ produced by photolysis of caged Ca2+. T his suggests that [Ca2+] gradients exist when Ca2+ is elevated by I(Ca ) and that, during Ca2+ entry, [Ca2+] at the activation site of the re lease channels must be much greater than spatially averaged [Ca2+] rep orted by the indicator. Analysis of voltage dependencies of I(Ca) inac tivation and SR Ca2+ release suggest that both Ca2+-dependent processe s are controlled by I(Ca) via the nearest T tubule Ca2+ channel rather than by total I(Ca) entry. The contribution of SR Ca2+ release to I(C a) inactivation studied with a two-pulse protocol was less than predic ted if Ca2+ derived from SR Ca2+ release and from T tubule Ca2+ channe ls have equal access to the Ca2+ binding site controlling I(Ca) inacti vation. These results can be explained in terms of a scheme where site s for release activation and I(Ca) inactivation are located in the sam e junctional gap subdomain, closer to the cytoplasmic mouth of the T t ubule Ca2+ channel than to the cytoplasmic mouth of the SR Ca2+ releas e channels. Such a scheme could provide an explanation for the graded nature and selective control of CICR in this preparation as well as in vertebrate cardiac muscle.