Am J Physiol Cell Physiol AJP citation statistics
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Am J Physiol Cell Physiol 252: C588-C594, 1987;
0363-6143/87 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Rasgado-Flores, H.
Right arrow Articles by Blaustein, M. P.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rasgado-Flores, H.
Right arrow Articles by Blaustein, M. P.

AJP - Cell Physiology, Vol 252, Issue 6 C588-C594, Copyright © 1987 by American Physiological Society


ARTICLES

ATP-dependent regulation of cytoplasmic free calcium in nerve terminals

H. Rasgado-Flores and M. P. Blaustein

ATP-dependent Ca uptake was studied in hyperpermeable (saponin treated) rat brain isolated nerve terminals (synaptosomes). The Ca uptake was measured at short incubation times (1-30 s) in the absence and presence of mitochondrial poisons, at various free Ca2+ concentrations (0.03-30 microM). Saponin treatment made the plasma membranes leaky without affecting the ATP-dependent Ca uptake by intracellular organelles. When the free Ca2+ concentration in the incubation medium was varied up to approximately 5 microM free Ca2+, mitochondrial blockers had no effect on the ATP-dependent Ca2+ uptake in the saponin-treated synaptosomes. At higher free Ca2+ concentrations, the blockers inhibited a portion of the ATP-dependent Ca uptake. This indicates that, in the dynamic physiological range of free Ca2+, the nonmitochondrial Ca uptake system (presumably the smooth endoplasmic reticulum, SER) is a more important Ca buffering system than the mitochondrial system. The SER sequesters Ca half maximally at free Ca2+ congruent to 0.4 microM and has a maximal Ca storage capacity of approximately 2 nmol/mg protein. The initial rate of SER Ca uptake is 0.1 nmol X mg protein-1 X s-1. This rate is too slow to account for the very rapid reduction of free Ca2+ that is required to terminate transmitter release immediately after presynaptic depolarization. Nevertheless, Ca sequestration in SER may play an important role in regulating longer term processes such as facilitation and post-tetanic potentiation.





HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online