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- W2040494057 abstract "We have recently shown that growth cones isolated from neonatal rat forebrain possess uptake and release mechanisms for the neurotransmitter γ-aminobutyric acid. About half of the K+-induced release of [3H]γ-aminobutyric acid from isolated growth cones is dependent on extracellular Ca2+. The remaining component of the [3H]γ-aminobutyric acid release is unaffected by removal of extracellular Ca2+ and is resistant to blockade by the voltage-sensitive Ca2+-channel blocker methoxyverapamil. In the present series of experiments we have used caffeine to assess the possible role of intracellular stores of Ca2+ in supporting that component of the K+-induced release of [3H]γ-aminobutyric acid from isolated growth cones that is independent of extracellular Ca2+. We have chosen caffeine because of its well established effect of releasing Ca2+ from smooth endoplasmic reticulum in muscle. We found that caffeine can release [3H]γ-aminobutyric acid from isolated growth cones. This effect persists in Ca2+-free medium, in the presence of methoxyverapamil and in the absence of Na+. Furthermore, isobutylmethylxanthine could not substitute for caffeine suggesting that the caffeine effect is not due to phosphodiesterase inhibition and the subsequent rise in intracellular cyclic nucleotides. A combination of the mitochondrial poisons, Antimycin A and sodium azide had no effect on the release of [3H]γ-aminobutyric acid induced either by caffeine or by high K+. We conclude that caffeine causes the release of Ca2+ from a non-mitochondrial store within the growth cone and that this Ca2+ store supports that component of the K+-induced release of [3H]γ-aminobutyric acid that is independent of extracellular Ca2+." @default.
- W2040494057 created "2016-06-24" @default.
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- W2040494057 date "1986-04-01" @default.
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- W2040494057 title "Further characterization of [3H]γ-aminobutyric acid release from isolated neuronal growth cones: Role of intracellular CA2+ stores" @default.
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- W2040494057 doi "https://doi.org/10.1016/0306-4522(86)90092-8" @default.
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