Abstract
Bay K 8644, nimodipine and ω-conotoxin GVIA (ω-CgTx) were used to study the different contribution of voltage-sensitive calcium channels (VSCC) to [ 3H]acetylcholine ([[ 3ACh) release in rat hippocampal synaptosomes. In our experimental conditions, the percentage of calcium-dependent ACh release was ~80%. Nimodipine (0.01–10 μM) and Bay K 8644 (0.01–10 μM) were not able to modify the [ 3H]ACh release under stimulating conditions (15 mM K +). Nevertheless, when K + concentration was reduced to 8 mM, a significant increase in [ 3H]ACh release was observed at 1 and 10 μM of Bay K 8644. Nimodipine (0.01–10 μM) failed to reverse the effect of Bay K 8644 on [ 3H]ACh release. Finally, ω-CgTx (0.001–1 μM) caused a concentration-dependent reduction of [ 3H]ACh release in K + (15 mM)-stimulating conditions. These results suggest that the N-type VSCC probably play a predominant role in regulating the [ 3H]ACh release in synaptosomes from rat hippocampus.
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