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首页> 外文期刊>Journal of Neurophysiology >On the origin of ultraslow spontaneous Na + fluctuations in neurons of the neonatal forebrain.
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On the origin of ultraslow spontaneous Na + fluctuations in neurons of the neonatal forebrain.

机译：关于新生儿前脑神经元超声自发Na +波动的起源。

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Spontaneous neuronal and astrocytic activity in the neonate forebrain is believed to drive the maturation of individual cells and their integration into complex brain-region-specific networks. The previously reported forms include bursts of electrical activity and oscillations in intracellular Ca~(2+)concentration. Here, we use ratiometric Na~(+)imaging to demonstrate spontaneous fluctuations in the intracellular Na~(+)concentration of CA1 pyramidal neurons and astrocytes in tissue slices obtained from the hippocampus of mice at postnatal days 2-4 (P2-4). These occur at very low frequency (～2/h), can last minutes with amplitudes up to several millimolar, and mostly disappear after the first postnatal week. To further investigate their mechanisms, we model a network consisting of pyramidal neurons and interneurons. Experimentally observed Na~(+)fluctuations are mimicked when GABAergic inhibition in the simulated network is made depolarizing. Both our experiments and computational model show that blocking voltage-gated Na~(+)channels or GABAergic signaling significantly diminish the neuronal Na~(+)fluctuations. On the other hand, blocking a variety of other ion channels, receptors, or transporters including glutamatergic pathways does not have significant effects. Our model also shows that the amplitude and duration of Na~(+)fluctuations decrease as we increase the strength of glial K~(+)uptake. Furthermore, neurons with smaller somatic volumes exhibit fluctuations with higher frequency and amplitude. As opposed to this, larger extracellular to intracellular volume ratio observed in neonatal brain exerts a dampening effect. Finally, our model predicts that these periods of spontaneous Na~(+)influx leave neonatal neuronal networks more vulnerable to seizure-like states when compared with mature brain. NEW & NOTEWORTHY Spontaneous activity in the neonate forebrain plays a key role in cell maturation and brain development. We report spontaneous, ultraslow, asynchronous fluctuations in the intracellular Na~(+)concentration of neurons and astrocytes. We show that this activity is not correlated with the previously reported synchronous neuronal population bursting or Ca~(2+)oscillations, both of which occur at much faster timescales. Furthermore, extracellular K~(+)concentration remains nearly constant. The spontaneous Na~(+)fluctuations disappear after the first postnatal week.
机译：新生儿前脑中自发的神经元和星形胶质细胞活动被认为推动单个细胞的成熟，并将其整合到复杂的大脑区域特定网络中。之前报道的形式包括电活动的爆发和细胞内Ca~（2+）浓度的振荡。在这里，我们使用比率Na~（+）成像来显示出生后第2-4天（P2-4）小鼠海马组织切片中CA1锥体神经元和星形胶质细胞的细胞内Na~（+）浓度的自发波动。这些现象发生频率很低（～2/h），可以持续几分钟，振幅高达几毫摩尔，在产后第一周后大部分消失。为了进一步研究它们的机制，我们建立了一个由锥体神经元和中间神经元组成的网络模型。当模拟网络中的GABA能抑制去极化时，模拟实验观察到的Na~（+）波动。我们的实验和计算模型都表明，阻断电压门控钠通道或GABA能信号显著降低神经元的钠离子波动。另一方面，阻断多种其他离子通道、受体或转运体（包括谷氨酸能途径）没有显著效果。我们的模型还表明，随着神经胶质细胞对钾离子摄取强度的增加，钠离子波动的幅度和持续时间都会减小。此外，体积较小的神经元表现出更高频率和振幅的波动。与此相反，在新生儿大脑中观察到的较大的细胞外与细胞内体积比发挥了抑制作用。最后，我们的模型预测，与成熟大脑相比，这些自发Na~（+）流入的周期使新生儿神经网络更容易出现癫痫样状态。新生儿前脑中新的和值得注意的自发活动在细胞成熟和大脑发育中起着关键作用。我们报告了神经元和星形胶质细胞内Na~（+）浓度的自发、超低、异步波动。我们发现，这种活动与之前报道的同步神经元群爆发或Ca~（2+）振荡无关，两者都发生在更快的时间尺度上。此外，细胞外K~（+）浓度几乎保持不变。出生后第一周，Na~（+）的自发波动消失。

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