| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Max-Volmer-Institut of Biophysical Chemistry, Technical University Berlin, Berlin, Germany
Correspondence: Address reprint requests to Dr. A. Knopp, AG Behr, Institute for Neurophysiology, Charité-Universitätsmedizin Berlin, Tucholskystr. 2, D-10117 Berlin, Germany. Tel.: 49-30-450 528209; Fax: 49-30-450 539941; E-mail: andreas.knopp{at}charite.de.
In vertebrate rod outer segments phototransduction is suggested to be modulated by intracellular Ca. We aimed at verifying this hypothesis by recording saturated photosignals in the rat retina after single and double flashes of light and determining the time tc to the beginning of the signal recovery. The time course of Cai after a flash was calculated from a change of the spatial Ca2+ concentration profile recorded in the space between the rods. After single flashes tc increased linearly with the logarithm of flash intensity, confirming the assumption that tc is determined by deactivation of a single species X* in the phototransduction cascade. The photoresponse was shortened up to 45% if the test flash was preceded by a conditioning preflash. The shortening depended on the reduction of Cai induced by the preflash. The data suggest that the phototransduction gain determining the amount of activated X* is regulated by a Cai-dependent mechanism in a short time period (<800 ms) after the test flash. Lowering of Cai by a preflash reduced the gain up to 20% compared to its value in a dark-adapted rod. The relation between phototransduction gain and Cai revealed a K1/2 value close to the dark level of Cai.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |