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首页> 外文期刊>American Journal of Physiology >Effect of chronically elevated CO2 on CA1 neuronal excitability.
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Effect of chronically elevated CO2 on CA1 neuronal excitability.

机译：长期升高的CO2对CA1神经元兴奋性的影响。

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To study the effect of chronically elevated CO(2) on the excitability and function of neurons, we exposed mice to 7.5-8% CO(2) for approximately 2 wk (starting at 2 days of age) and examined the properties of freshly dissociated hippocampal neurons. Neurons from control mice (CON) and from mice exposed to chronically elevated CO(2) had similar resting membrane potentials and input resistances. CO(2)-exposed neurons, however, had a lower rheobase and a higher Na(+) current density (580 +/- 73 pA/pF; n = 27 neurons studied) than did CON neurons (280 +/- 51 pA/pF, n = 34; P < 0.01). In addition, the conductance-voltage curve was shifted in a more negative direction in CO(2)-exposed than in CON neurons (midpoint of the curve was -46 +/- 3 mV for CO(2) exposed and -34 +/- 3 mV for CON, P < 0.01), while the steady-state inactivation curve was shifted in a more positive direction in CO(2)-exposed than in CON neurons (midpoint of the curve was -59 +/- 2 mV for CO(2) exposed and -68 +/- 3 mV for CON, P < 0.01).The time constant for deactivation at -100 mV was much smaller in CO(2)-exposed than in CON neurons (0.8 +/- 0.1 ms for CO(2) exposed and 1.9 +/- 0.3 ms for CON, P < 0.01). Immunoblotting for Na(+) channel proteins (subtypes I, II, and III) was performed on the hippocampus. Our data indicate that Na(+) channel subtype I, rather than subtype II or III, was significantly increased (43%, n = 4; P < 0.05) in the hippocampi of CO(2)-exposed mice. We conclude that in mice exposed to elevated CO(2), 1) increased neuronal excitability is due to alterations in Na(+) current and Na(+) channel characteristics, and 2) the upregulation of Na(+) channel subtype I contributes, at least in part, to the increase in Na(+) current density.
机译：要研究慢性升高的CO（2）对神经元兴奋性和功能的影响，我们将小鼠暴露于7.5-8％CO（2）约2周（从2天龄开始），并检查了新鲜离解的特性海马神经元。来自控制小鼠（CON）和暴露于慢性升高CO（2）的小鼠的神经元具有相似的静息膜电位和输入阻力。但是，与CON神经元（280 +/- 51 pA）相比，暴露于CO（2）的神经元具有较低的流变碱和较高的Na（+）电流密度（580 +/- 73 pA / pF; n =研究的27个神经元）。 / pF，n = 34; P <0.01）。此外，电导率-电压曲线在暴露于CO（2）的情况下比在CON神经元中向负方向移动更多（对于暴露于CO（2）和-34 + /，曲线的中点为-46 +/- 3 mV -CON为3 mV，P <0.01），而在CO（2）暴露下，稳态灭活曲线的移动方向比CON神经元大（正中点为-59 +/- 2 mV）暴露的CO（2）和CON的-68 +/- 3 mV，P <0.01）。暴露于CO（2）的钝化时间为-100 mV的时间常数比CON神经元小得多（0.8 +/- 0.1暴露的CO（2）的毫秒数（ms）和CON（1.9 +/- 0.3毫秒），P <0.01）。 Na（+）通道蛋白（I，II和III型）的免疫印迹是在海马体上进行的。我们的数据表明，在暴露于CO（2）的小鼠海马体中，Na（+）通道亚型I而不是亚型II或III显着增加（43％，n = 4; P <0.05）。我们得出的结论是，在暴露于升高的CO（2）的小鼠中，1）神经元兴奋性增加是由于Na（+）电流和Na（+）通道特征的改变，以及2）Na（+）通道亚型I的上调至少部分是因为Na（+）电流密度的增加。

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