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神经元输入通过少突胶质细胞中的 AMPA 受体和电压门控钙通道触发 Ca2+内流。

Neuronal input triggers Ca influx through AMPA receptors and voltage-gated Ca channels in oligodendrocytes.

机构信息

Department of Cellular and Integrative Physiology, UT Health San Antonio, San Antonio, Texas.

出版信息

Glia. 2019 Oct;67(10):1922-1932. doi: 10.1002/glia.23670. Epub 2019 Jul 17.

DOI:10.1002/glia.23670
PMID:31313856
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6771819/
Abstract

Communication between neurons and developing oligodendrocytes (OLs) leading to OL Ca rise is critical for axon myelination and OL development. Here, we investigate signaling factors and sources of Ca rise in OLs in the mouse brainstem. Glutamate puff or axon fiber stimulation induces a Ca rise in pre-myelinating OLs, which is primarily mediated by Ca -permeable AMPA receptors. During glutamate application, inward currents via AMPA receptors and elevated extracellular K caused by increased neuronal activity collectively lead to OL depolarization, triggering Ca influx via P/Q- and L-type voltage-gated Ca (Ca ) channels. Thus, glutamate is a key signaling factor in dynamic communication between neurons and OLs that triggers Ca transients via AMPARs and Ca channels in developing OLs. The results provide a mechanism for OL Ca dynamics in response to neuronal input, which has implications for OL development and myelination.

摘要

神经元和发育中的少突胶质细胞(OLs)之间的通讯导致 OLs 的 Ca 上升,这对于轴突髓鞘形成和 OL 的发育至关重要。在这里,我们研究了小鼠脑干中 OL 中 Ca 上升的信号因子和来源。谷氨酸脉冲或轴突纤维刺激诱导前髓鞘化 OL 中的 Ca 上升,这主要是由 Ca 通透性 AMPA 受体介导的。在谷氨酸应用过程中,通过 AMPA 受体的内向电流和由于神经元活动增加而导致的细胞外 K 升高共同导致 OL 去极化,通过 P/Q-和 L-型电压门控 Ca(Ca )通道触发 Ca 内流。因此,谷氨酸是神经元和 OL 之间动态通讯的关键信号因子,通过 AMPAR 和发育中的 OL 中的 Ca 通道触发 Ca 瞬变。研究结果为 OL 对神经元输入的 Ca 动力学提供了一种机制,这对 OL 的发育和髓鞘形成具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/f3a45cc4ae5e/GLIA-67-1922-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/028b37cfc6b2/GLIA-67-1922-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/ca1fb81acb7e/GLIA-67-1922-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/9fef8d5a936e/GLIA-67-1922-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/40324b7d044d/GLIA-67-1922-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/7c7ba1e929bc/GLIA-67-1922-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/f3a45cc4ae5e/GLIA-67-1922-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/028b37cfc6b2/GLIA-67-1922-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/ca1fb81acb7e/GLIA-67-1922-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/9fef8d5a936e/GLIA-67-1922-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/40324b7d044d/GLIA-67-1922-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/7c7ba1e929bc/GLIA-67-1922-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/abde/6771819/f3a45cc4ae5e/GLIA-67-1922-g006.jpg

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