Organic calcium channel blockers enhance [3H]purine release from rat brain cortical synaptosomes |
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Authors: | P H Wu M Moron Dr R Barraco |
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Institution: | (1) Department of Physiology, Wayne State University School of Medicine, 540 E. Canfield Ave., 48201 Detroit, Michigan;(2) Present address: Clinical Institute, Addiction Research Foundation, 33 Russell St., M5S 2S1 Toronto, Ontario, Canada |
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Abstract: | The release of 3H]purines was investigated in a crude mitochondrial fraction (P2 fraction) from rat brain cortex pre-loaded with 3H]adenosine for 30 sec at 37°C in vitro. Potassium, veratridine and glutamate were used as depolarizing agents to evoke the release of 3H]purines. Ca2+ removal, the addition of EGTA, and treatment with organic or inorganic Ca2+ antagonists did not inhibit 3H]purine release in this preparation. On the other hand, Ca2+ removal and the addition of EGTA greatly enhanced3H-purine release induced by glutamate. D-600 and diltiazem enhanced K+-evoked 3H]purine release, and nifedipine increased veratridine evoked 3H]purine release indicating that either these Ca2+ antagonists have different sites of action, or that K+ and veratridine may release 3H]purine from different metabolic pools. Organic Ca2+ antagonists failed to enhance the 3H]purine release evoked by glutamate, further supporting the notion that various depolarizing agents may release 3H]purines from different cellular compartments. |
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