Constraints of vigilance-dependent noradrenergic signaling to mouse cerebellar Bergmann glia.

Constraints of vigilance-dependent noradrenergic signaling to mouse cerebellar Bergmann glia.
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警惕依赖性去甲肾上腺素能信号对小鼠小脑伯格曼神经胶质细胞的限制。

DOI:
10.1002/glia.24350
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发表时间:
2023
期刊:
影响因子:
6.2
通讯作者:
Paukert,Martin
Paukert,Martin
中科院分区:
医学1区
文献类型:
--
作者:
Salinas-Birt,Angelica;Zhu,Xiangyu;Lim,EuniceY;CruzSantory,AryanaJ;Ye,Liang;Paukert,Martin

文献摘要

相似文献

行为状态在决定星形胶质细胞钙信号中起着重要作用。特别是,运动介导的警觉性提高已被发现触发整个大脑星形胶质细胞中去甲肾上腺素依赖的全细胞钙离子升高。最近发现,对于小脑Bergmann胶质细胞,运动诱导的瞬时钙升高依赖于它们的α1A-肾上腺素能受体。随着运动作为行为参数的应用越来越广泛,了解去甲肾上腺素信号对星形胶质细胞的制约变得越来越重要。在这里,我们评估了运动速度、持续时间和间隔时间对Bergmann胶质细胞和小脑去甲肾上腺素能轴突终末钙信号的影响。我们发现运动速度几乎不依赖于运动速度,但在最初的钙瞬时延长运动事件之后,显示出稳态的钙升高。比较瞬时Bergmann神经胶质细胞和去甲肾上腺素能终末Ca~(2+)动力学变化的时程和恢复,表明去甲肾上腺素能终末Ca~(2+)活性决定了Bergmann神经胶质细胞的激活,不需要去甲肾上腺素受体脱敏来解释长时间运动中的衰减。进一步分析观察区域内钙动态变化之间的相关性,我们发现去甲肾上腺素能终末之间的协调活动可以解释稳态Bergmann胶质细胞钙活性的波动。总之,我们的发现将有助于更好地理解较不受控制的觉醒行为中星形胶质细胞钙离子的动态变化,并可能指导更好地依赖于星形胶质细胞钙信号的行为背景的识别。
Behavioral state plays an important role in determining astroglia Ca2+signaling. In particular, locomotion‐mediated elevated vigilance has been found to trigger norepinephrine‐dependent whole cell Ca2+elevations in astroglia throughout the brain. For cerebellar Bergmann glia it has recently been found that locomotion‐induced transient Ca2+elevations depend on their α1A‐adrenergic receptors. With increasing availability and implementation of locomotion as behavioral parameter it becomes important to understand the constraints of noradrenergic signaling to astroglia. Here we evaluated the effect of speed, duration and interval of locomotion on Ca2+signals in Bergmann glia as well as cerebellar noradrenergic axon terminals. We found almost no dependence on locomotion speed, but following the initial Ca2+transient prolonged locomotion events revealed a steady‐state Ca2+elevation. Comparison of time course and recovery of transient Bergmann glia and noradrenergic terminal Ca2+dynamics suggested that noradrenergic terminal Ca2+activity determines Bergmann glia Ca2+activation and does not require noradrenergic receptor desensitization to account for attenuation during prolonged locomotion. Further, analyzing the correlation among Ca2+dynamics within regions within the field of observation we found that coordinated activity among noradrenergic terminals accounts for fluctuations of steady‐state Bergmann glia Ca2+activity. Together, our findings will help to better understand astroglia Ca2+dynamics during less controlled awake behavior and may guide the identification of behavioral contexts preferably dependent on astroglia Ca2+signaling.