Characterization of divalent cation-induced [3H]Acetylcholine release from EGTA-treated rat hippocampal synaptosomes |
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Authors: | Thomas W Vickroy Cynthia J Schneider |
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Institution: | (1) Departments of Physiological Sciences, University of Florida, Box J-144 J.H.M.H.C., 32610 0144 Gainesville, Florida;(2) Neuroscience, University of Florida, Box J-144 J.H.M.H.C., 32610 0144 Gainesville, Florida |
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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 10M EGTA), calcium reversibly increased 3H]acetylcholine efflux (up to five-fold) while causing no measurable efflux of lactate dehydrogenase. When substituted for calcium, strongtium 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 -conotoxin but were insensitive to nifedipine and cobalt (both 10 M). In addition, stimulation of muscarnic 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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Keywords: | Acetylcholine barium calcium EGTA synaptosomes cation channels |
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