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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Intra- vs extracellular calcium regulation of neurotransmitter-stimulated phosphoinositide breakdown.
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Intra- vs extracellular calcium regulation of neurotransmitter-stimulated phosphoinositide breakdown.

机译：神经递质刺激的磷酸肌醇分解的细胞内和细胞外钙调节。

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摘要

The dependence on Ca2+ of basal, glutamate- and carbachol-stimulated phosphoinositide (PI) turnover was studied on 8-day old rat brain synaptoneurosomes. For that purpose, intracellular and extracellular Ca2+ concentrations were buffered by bis-(alpha-aminophenoxy)-ethane-N,N,N',N'-tetraacetic acid, in its tetra(acetoxymethyl)-ester form (BAPTA-AM) and in its free acid form (BAPTA), respectively. The effects of both forms of the calcium chelator intracellular and extracellular Ca2+ buffering on intracellular and extracellular Ca2+ concentration ([Ca2+]i and [Ca2+]e) were determined with fluorimetric assay using fura2, either in its acetoxymethyl ester form (fura2-AM) or in its free acid form. Intracellular chelation of Ca2+ ions with BAPTA-AM induced a dose-dependent reduction of the [Ca2+]i. Basal inositol phosphate (IP) formation was slightly affected by this [Ca2+]i buffering, while glutamate and carbachol stimulations of PI hydrolysis were similarly diminished. Chelation of extracellular Ca2+ ions with BAPTA produced a reduction of both [Ca2+]e and [Ca2+]i. Basal IP accumulation was maximally inhibited by 50%. The carbachol-induced PI hydrolysis was completely inhibited in the presence of 200 microM BAPTA, while a substantial residual glutamate-elicited IP response remained (40% of the control response). It is concluded that [Ca2+]i of synaptoneurosomes is not critical for basal and neurotransmitter-stimulated IP formation, whilst [Ca2+]e is critical. Glutamate may, in part, stimulate PI breakdown in a Ca(2+)-insensitive way.
机译：在8天大的大鼠脑突触小体上研究了基础，谷氨酸和卡巴胆碱刺激的磷酸肌醇（PI）转换对Ca2 +的依赖性。为此目的，细胞内和细胞外Ca2 +的浓度由双（α-氨基苯氧基）-乙烷-N，N，N'，N'-四乙酸酯以四（乙酰氧基甲基）酯形式（BAPTA-AM）和分别为游离酸形式（BAPTA）。钙螯合剂两种形式的胞内和胞外Ca2 +缓冲液对胞内和胞外Ca2 +浓度（[Ca2 +] i和[Ca2 +] e）的影响通过使用呋喃2的荧光测定法（以乙酰氧基甲基酯形式（fura2-AM））测定。或呈游离酸形式。 BAPTA-AM对Ca2 +离子进行细胞内螯合可诱导[Ca2 +] i的剂量依赖性降低。基础肌醇磷酸酯（IP）的形成受[Ca2 +] i缓冲作用的轻微影响，而谷氨酸和卡巴胆碱对PI水解的刺激作用也同样减弱。用BAPTA螯合细胞外Ca2 +离子可减少[Ca2 +] e和[Ca2 +] i。基础IP累积被最大抑制了50％。在200 microM BAPTA的存在下，完全抑制了卡巴胆碱诱导的PI水解，而残留的大量谷氨酸引发的IP反应仍然存在（占对照反应的40％）。结论是，突触神经小体的[Ca2 +] i对基础和神经递质刺激的IP形成并不关键，而[Ca2 +] e则至关重要。谷氨酸盐可能部分以Ca（2+）不敏感的方式刺激PI分解。

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