Changes in Membrane Potential and the Intracellular Calcium Concentration During CSD and OGD in Layer V and Layer II/III Mouse Cortical Neurons
Changes in Membrane Potential and the Intracellular Calcium Concentration During CSD and OGD in Layer V and Layer II/III Mouse Cortical Neurons
复制标题
DOI：
10.1152/jn.00922.2009
复制
发表时间：
2010-12-01
影响因子：
2.5
通讯作者：
Martin, Rosemary L.
中科院分区：
文献类型：
--
作者：
Gniel, Helen M.;Martin, Rosemary L.
Gniel HM，Martin RL.CSD和OGD过程中V层和II/III层小鼠皮质神经元膜电位和细胞内钙离子浓度的变化。神经生理学杂志104：3203-3212,2010。2010年9月1日首次出版；DOI：10.1152/jn.00922.2009。皮质扩散性抑制(CSD)是在强烈的神经元活动后的一段电沉默，这种活动以类似于3-6 mm/min的速度传播穿过皮质，并与短暂的神经元去极化有关。CSD在正常灌注的脑组织中是良性的，但有证据表明，重复性CSD有助于局灶性脑缺血后梗塞的扩大。到目前为止，研究假设CSD的细胞反应在不同的神经元类型中是一致的，因为没有相反的数据。本研究观察了CSD对小鼠脑片V层和II/III层锥体细胞膜电位和细胞内钙离子浓度([Ca~(2+)](I))的影响。为了将数据放在背景中，我们在缺氧和葡萄糖剥夺(OGD)诱导的缺氧性去极化过程中进行了类似的测量。用低亲和力比率指示剂Fura-4F测定[Ca~(2+)](I)。在CSD和OGD诱导的去极化过程中，所有神经元的膜电位均接近0 mV。在V层锥体，OGD导致[Ca~(2+)](I)增加到最大值3.69+/-0.73(SD)muM(n=12)，显著大于CSD的增加(n=34；P<；0.0001)。膜电位和[Ca~(2+)](I)在CSD后恢复到接近基础水平，但未恢复到OGD的基础水平。II/III层神经元对CSD有反应，[Ca~(2+)](I)峰值升高幅度大于V层神经元(2.88+/-0.6µM；n=9；P<；0.01)。我们得出结论，锥体神经元对CSD的反应存在层流差异；讨论了可能的解释。
Gniel HM, Martin RL. Changes in membrane potential and the intracellular calcium concentration during CSD and OGD in layer V and layer II/III mouse cortical neurons. J Neurophysiol 104: 3203-3212, 2010. First published September 1, 2010; doi:10.1152/jn.00922.2009. Cortical spreading depression (CSD) is an episode of electrical silence following intense neuronal activity that propagates across the cortex at similar to 3-6 mm/min and is associated with transient neuronal depolarization. CSD is benign in normally perfused brain tissue, but there is evidence suggesting that repetitive CSD contributes to infarct growth following focal ischemia. Studies to date have assumed that the cellular responses to CSD are uniform across neuronal types because there are no data to the contrary. In this study, we investigated the effect of CSD on membrane potential and the intracellular calcium concentration ([Ca2+](i)) of mouse layer V and layer II/III pyramidal neurons in brain slices. To place the data in context, we made similar measurements during anoxic depolarization induced by oxygen and glucose deprivation (OGD). The [Ca2+](i) was quantified using the low-affinity ratiometric indicator Fura-4F. During both CSD- and OGD-induced depolarization, the membrane potential approached 0 mV in all neurons. In layer V pyramids OGD resulted in an increase in [Ca2+](i) to a maximum of 3.69 +/- 0.73 (SD) mu M (n = 12), significantly greater than the increase to 1.81 +/- 0.70 mu M in CSD (n = 34; P < 0.0001). Membrane potential and [Ca2+](i) returned to nearly basal levels following CSD but not OGD. Layer II/III neurons responded to CSD with a greater peak increase in [Ca2+](i) than layer V neurons (2.88 +/- 0.6 mu M; n = 9; P < 0.01). We conclude there is a laminar difference in the response of pyramidal neurons to CSD; possible explanations are discussed.