Two mechanisms that raise free intracellular calcium in rat hippocampal neurons during hypoosmotic and low NaCl treatment
Two mechanisms that raise free intracellular calcium in rat hippocampal neurons during hypoosmotic and low NaCl treatment
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DOI：
10.1152/jn.2000.83.1.81
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发表时间：
2000-01-01
影响因子：
2.5
通讯作者：
Wadman, WJ
中科院分区：
文献类型：
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作者：
Borgdorff, AJ;Somjen, GG;Wadman, WJ
先前的研究表明，将海马切片暴露于低渗透压（pi(o)）或低细胞外氯化钠浓度（[NaCl](o)）会增强突触传递，并导致间质钙（[Ca2+](o)）减少。 [Ca2+](0) 的减少表明细胞摄取并可以解释突触传递的增强。我们使用荧光指示染料测量细胞内钙活性 ([Ca2+](i))。在组织切片中的 CA1 海马锥体神经元中，将 pi(o) 降低约 70 mOsm 会导致“静息”[Ca2+](i) 以及突触或直接刺激的钙活性瞬时增加 (Delta[Ca2+](i)) 短暂减少然后增加。在分离的细胞中，将 sr 降低约 70 mOsm 会导致 [Ca2+](i) 平均几乎翻倍，从 83 nM 降至 155 nM。 [Ca2+](i) 的增加与低渗细胞肿胀没有显着相关性。等渗（甘露醇或蔗糖取代）降低 [NaCl](o) 不会导致细胞肿胀，但也会升高 [Ca2+](i)。用胆碱-Cl 或甲基硫酸钠替代 NaCl 不会影响 [Ca2+](i)。在浸泡在无钙培养基中的神经元中，降低 pi(o) 会导致 [Ca2+](i) 轻度增加，这与细胞肿胀有关，但在没有外部 Ca2+ 的情况下，[NaCl](o) 的等渗降低仅引发短暂的瞬时反应。我们得出的结论是，细胞外离子强度的降低（即低 pi(o) 和低 [NaCl](o)）会导致 Ca2+ 从细胞外介质净流入，而细胞肿胀或膜张力增加是细胞内储备释放 Ca2+ 的信号。
Previous studies have shown that exposing hippocampal slices to low osmolarity (pi(o)) or to low extracellular NaCl concentration ([NaCl](o)) enhances synaptic transmission and also causes interstitial calcium ([Ca2+](o)) to decrease. Reduction of [Ca2+](0) suggests cellular uptake and could explain the potentiation of synaptic transmission. We measured intracellular calcium activity ([Ca2+](i)) using fluorescent indicator dyes. In CAl hippocampal pyramidal neurons in tissue slices, lowering pi(o) by similar to 70 mOsm caused "resting" [Ca2+](i) as well as synaptically or directly stimulated transient increases of calcium activity (Delta[Ca2+](i)) to transiently decrease and then to increase. In dissociated cells, lowering sr,by similar to 70 mOsm caused [Ca2+](i) to almost double on average from 83 to 155 nM. The increase of [Ca2+](i) was not significantly correlated with hypotonic cell swelling. Isoosmotic (mannitol- or sucrose-substituted) lowering of [NaCl](o), which did not cause cell swelling, also raised [Ca2+](i). Substituting NaCl with choline-Cl or Na methyl-sulfate did not affect [Ca2+](i). In neurons bathed in calcium-free medium, lowering pi(o) caused a milder increase of [Ca2+](i), which was con-elated with cell swelling, but in the absence of external Ca2+, isotonic lowering of [NaCl](o) triggered only a brief, transient response. We conclude that decrease of extracellular ionic strength (i.e., in both low pi(o) and low [NaCl](o)) causes a net influx of Ca2+ from the extracellular medium whereas cell swelling, or the increase in membrane tension, is a signal for the release of Ca2+ from intracellular stores.