Regulation of cytosolic calcium concentration in presynaptic nerve endings isolated from rat brain.
Regulation of cytosolic calcium concentration in presynaptic nerve endings isolated from rat brain.
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大鼠脑突触前神经末梢胞质钙浓度的调节。
DOI：
10.1113/jphysiol.1985.sp015697
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
Nachshen,DA
中科院分区：
文献类型：
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作者：
Nachshen,DA
用荧光钙指示剂quin2研究了从大鼠脑分离的突触前神经末梢（突触体）中胞浆钙浓度（[Ca]i）的调节。在含有1‐2 mM‐Ca的溶液中，静息[Ca]i为0.1‐0.2微米。当外部Ca浓度从0.02 mM增加到2 mM时，[Ca]i仅增加100 ~ 150 nM，而线粒体抑制剂valinomycin和氟羰基氰苯腙（FCCP）使[Ca]i增加100 ~ 200 nM。这种增加与添加抑制剂之前的[Ca]i的静息水平无关，但它取决于外部Ca的存在。这些抑制剂对[Ca]i的影响似乎可能是代谢抑制的次要后果。当外部Na浓度从145 mM降低到5 mM时，[Ca]i增加约2倍，当外部Na浓度恢复时，[Ca]i恢复到初始水平。这种恢复也发生在FCCP存在的情况下。这些结果表明，Na/Ca交换，而不是线粒体Ca摄取，在调节[Ca]i和允许神经末梢从Ca负荷中恢复中起作用。
The regulation of cytosolic Ca concentration ([Ca]i) was studied with the fluorescent Ca indicator, quin2, in pinched‐off presynaptic nerve endings (synaptosomes) isolated from rat brain. The resting [Ca]i is 0.1‐0.2 microM, in solutions containing 1‐2 mM‐Ca. [Ca]i increases by only 100‐150 nM when the external Ca concentration is increased from 0.02 to 2 mM. The mitochondrial inhibitors valinomycin and fluoro‐carbonyl cyanide phenylhydrazone (FCCP) increase [Ca]i by 100‐200 nM. This increase is not correlated with the resting level of [Ca]i prior to the addition of inhibitors, but it is dependent on the presence of external Ca. It seems likely that the effect of these inhibitors on [Ca]i is a secondary consequence of metabolic inhibition. [Ca]i increases by about 2‐fold when the external Na concentration is lowered from 145 to 5 mM, and returns to its initial level when external Na is restored. This recovery occurs also in the presence of FCCP. These results suggest that Na/Ca exchange, but not mitochondrial Ca uptake, plays a role in regulating [Ca]i and in allowing the nerve terminals to recover from Ca loading.