Premium
Stimulation of calcium‐dependent release of labelled protein from pulse‐labelled mouse pituitary intermediate lobe tissue
Author(s) -
Thornton V. F.
Publication year - 1982
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1982.sp014311
Subject(s) - depolarization , stimulation , chemistry , verapamil , calcium , biophysics , pulse (music) , medicine , endocrinology , biology , organic chemistry , engineering , detector , electrical engineering
1. The effect of K depolarization on the release of labelled protein from pulse‐labelled intermediate lobe tissue of mouse pituitaries has been studied. 2. Depolarization briefly stimulated Ca‐dependent release of labelled protein. Co (2·5 mM) and verapamil (0·08 mM) reversibly blocked stimulation. Efflux of 45 Ca was also briefly stimulated by depolarization, but not in the presence of Co or verapamil, nor in the absence of Ca. 3. The response to maintained depolarization quickly inactivated. Inactivation probably resulted from Ca‐channel inactivation rather than exhaustion of available labelled protein, since responses different in magnitude but of constant time course could be obtained by depolarization in different concentrations of Ca. In addition, much more labelled protein could be released by exposure to Ba. 4. Depolarization did not cause a response if the Ca concentration was 0·4 mM or less; neither did inactivation occur in these conditions, and a response occurred as soon as the Ca concentration was raised. Two separate responses could be generated by a stepwise increase in the Ca concentration during maintained depolarization. The magnitude of the two responses together was similar to the magnitude of one response at the higher Ca concentration. 5. Recovery from inactivation was complete after about 20 min in normal K. However, recovery also occurred during maintained depolarization provided the Ca concentration was reduced sufficiently. Recovery was complete at 0·4 mM‐Ca or less, and at higher concentrations the extent of recovery depended on the Ca concentration selected. 6. It is concluded that depolarization opened potential‐dependent Ca channels permitting Ca entry and causing the release of labelled products. The response was brief probably because the Ca channels were inactivated. Since the channels were not inactivated by depolarization in low Ca, inactivation may result from Ca entry.