Calcium mobilization from the intracellular mitochondrial and nonmitochondrial stores of the rat cerebellum

• Published in: Brain research 1996-04, Vol.718 (1), p.151-158
• Main Authors: Huang, Wei-Cherng, Chueh, Sheau-Huei
• Format: Article
• Language: English
• Subjects: Animals; Arachidonic acid; Arachidonic Acids - pharmacology; Biochemistry and metabolism; Biological and medical sciences; Ca 2+ mobilization; Calcium - metabolism; Calcium Channel Blockers - pharmacology; Central nervous system; Cerebellum - drug effects; Cerebellum - metabolism; Cerebellum - ultrastructure; Fundamental and applied biological sciences. Psychology; In Vitro Techniques; Intracellular Ca 2+ pool; Male; Membranes - drug effects; Membranes - metabolism; Microsomes - drug effects; Microsomes - metabolism; Mitochondria; Mitochondria - drug effects; Mitochondria - metabolism; Phosphorylcholine - analogs & derivatives; Phosphorylcholine - pharmacology; Rats; Rats, Sprague-Dawley; Ruthenium Red - pharmacology; Sphingosine; Sphingosine - analogs & derivatives; Sphingosine - pharmacology; Sphingosylphosphorylcholine; Tumor Cells, Cultured; Vertebrates: nervous system and sense organs
• ISSN: 0006-8993; 1872-6240
• DOI: 10.1016/0006-8993(96)00108-4

Two major intracellular Ca 2+ stores, the mitochondrial and nonmitochondrial (microsomes) fractions isolated from rat cerebellum, exhibited a Ca 2+ concentration and ATP-dependent Ca 2+ accumulation. The maximal Ca 2+ accumulation in mitochondria was higher than in microsomes, but the affinity of the mitochondria for Ca 2+ was lower. In this study, Ca 2+ accumulation within the mitochondria was energized by ATP hydrolysis. Thus, the protonophore, carbonyl cyanide p-trifluoromethoxyphenylhydrazone, and the F 1F 0 ATP synthase inhibitor, oligomycin, blocked Ca 2+ accumulation and induced the discharge of the entrapped Ca 2+ in the mitochondria, whereas the metabolic inhibitor, rotenone, affected neither the Ca 2+ accumulation nor discharge. On the other hand, the uniporter inhibitor, ruthenium red, blocked the mitochondrial accumulation of Ca 2+, but did not cause the discharge of preloaded Ca 2+. In addition, arachidonic acid (AA), sphingosylphosphorylcholine (SPC) and sphingosine (SPH) elicited the dose-dependent release of Ca 2+ from microsomel stores. Although the magnitudes of the Ca 2+ release induced by AA, SPC or SPH were all dependent on the presence of extravesicular Ca 2+ at concentrations ranging from 0.01 to 0.1 μM Ca 2+, only the AA- and SPC-evoked Ca 2+ releases were insensitive to temperature. The mitochondria were more sensitive than the microsomes to the AA induced release of accumulated Ca 2+. Our results indicate the existence of multiple intracellular Ca 2+ stores in nerve cells which can be released by various Ca 2+ mediators.