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Synaptosomal Calcium Uptake Systems: Prostaglandins Are Probably Not Involved in the Regulation of Calcium Fluxes Into and Within the Nerve Endings
Author(s) -
Denzlinger Claudio,
Hertting Georg,
Jackisch Rolf
Publication year - 1982
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1111/j.1471-4159.1982.tb03972.x
Subject(s) - free nerve ending , synaptosome , calcium , chemistry , lysis , biochemistry , mitochondrion , ouabain , biophysics , organelle , prostaglandin , efflux , endocrinology , sodium , biology , organic chemistry
Abstract:45 Ca 2+ uptake measurements were performed on intact and osmotically lysed synaptosomes from rat brain to study the possible influence of prostaglandins (PGs) on Ca 2+ movements into and within the nerve endings. The K + ‐induced 45 Ca 2+ uptake of intact synaptosomes was not influenced by several inhibitors of PG synthesis. 45 Ca 2+ uptake in lysed synaptosomal preparations was promoted by ATP and seemed to be largely attributable to mitochondria, as it was inhibited by mitochondrial poisons. This Ca 2+ uptake was strongly reduced by PG synthesis inhibitors but also by PG precursor fatty acids. Both PG synthesis inhibitors and precursors, according to their relative efficacy in blocking Ca 2+ uptake, were able to induce Ca 2+ efflux from preloaded intrasynaptosomal organelles. The PGs E 2 , F 2α , D 2 , and thromboxane B 2 were without effect on 45 Ca 2+ uptake in lysed synaptosomal preparations. On the basis of our results it does not seem likely that PGs influence Ca 2+ availability by modulating Ca 2+ fluxes into or within the nerve endings. The observed inhibitory effects of PG synthesis inhibitors and precursors on the intrasynaptosomal Ca 2+ uptake might be due to unspecific impairment of mitochondrial functions.