ArticleNeurochemical research1991
Characterization of divalent cation-induced [3H]acetylcholine release from EGTA-treated rat hippocampal synaptosomes.
Article in Neurochemical research, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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0 citing papers in PubMed, 8 citations in OpenAlex.
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2 authors at 1 institution in 2 countries.
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Abstract
Calcium-naive synaptosomes were used to assess the effects of divalent cations on [3H]acetylcholine release from rat hippocampal homogenates. Following equilibration with calcium-free buffer (containing 10 microM EGTA), calcium reversibly increased [3H]acetylcholine efflux (up to five-fold) while causing no measurable efflux of lactate dehydrogenase. When substituted for calcium, strontium and barium behaved similarly although barium exhibited three-fold greater efficacy. In the presence of elevated potassium, 4-aminopyridine or tetraethylammonium, the secretagogue efficacy of calcium (but not barium) was markedly increased. The release-promoting effects of both cations were inhibited by lanthanum, magnesium, cadmium, and omega-conotoxin but were insensitive to nifedipine and cobalt (both 10 microM). In addition, stimulation of muscarinic cholinergic autoreceptors substantially inhibited both calcium and barium-evoked [3H]acetylcholine release. Taken together, these results indicate that cation-evoked transmitter release from calcium-naive synaptosomes is subject to normal neuroregulatory mechanisms and therefore should be useful for investigating presynaptic modulation of neuronal exocytosis.
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