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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Molecular mechanisms of microglial activation. B. Voltage- and purinoceptor-operated channels in microglia.
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Molecular mechanisms of microglial activation. B. Voltage- and purinoceptor-operated channels in microglia.

机译：小胶质细胞活化的分子机制。 B.小胶质细胞中电压和嘌呤受体操纵的通道。

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Cultured, proliferating microglial cells can be further activated by lipopolysaccharide (LPS) and, thereby, turned into a non-proliferating state. While proliferating cells exhibit only inwardly rectifying potassium channels, non-proliferating cells express, in addition, outwardly rectifying potassium channels. The characteristics of the two channel populations are markedly different. Inward potassium currents inactivate and can be abolished by extracellular Cs+ and Ba2+. Outward potassium currents only slightly inactivate and can be abolished by 4-aminopyridine, quinine and charybdotoxin. An increase in the intracellular free Ca2+ concentration depresses the outward potassium current. ATP or its structural analogues stimulate two types of P2-purinoceptors on microglial cells, a ligand-activated cationic channel (P2x) which produces depolarization and a G protein coupled receptor (P2Y) which produces hyper-polarization via the opening of K+ channels. Both P2X- and P2Y-receptor stimulation may increase the intracellular Ca2+ concentration. In the former case, Ca2+ enters the cells via non-selective cationic channels. In the latter case, Ca2+ may be released from intracellular stores, owing to activation of the enzyme phospholipase C and subsequent generation of inositol 1,4,5-trisphosphate (IP3). It is assumed that neuronal damage leads to efflux of ATP into the extracellular space with subsequent activation of microglia. ATP-induced excessive depolarizations by P2X-purinoceptor stimulation may be counteracted by outwardly rectifying potassium channels and by hyperpolarizing P2Y-purinoceptors in non-proliferating microglia.
机译：培养的增殖性小胶质细胞可以被脂多糖（LPS）进一步激活，从而变成非增殖状态。尽管增殖细胞仅表现出向内整流的钾通道，但非增殖细胞还表达向外整流的钾通道。两个渠道人口的特征明显不同。内向钾电流失活，可被细胞外Cs +和Ba2 +消除。外向钾电流仅略微失活，可被4-氨基吡啶，奎宁和炭疽毒素消除。细胞内游离Ca 2+浓度的增加抑制了向外的钾电流。 ATP或它的结构类似物刺激小胶质细胞上的两种P2-嘌呤受体，配体激活的阳离子通道（P2x）产生去极化，而G蛋白偶联受体（P2Y）则通过打开K +通道产生超极化。 P2X和P2Y受体刺激均可增加细胞内Ca2 +浓度。在前一种情况下，Ca2 +通过非选择性阳离子通道进入细胞。在后一种情况下，由于磷脂酶C的活化和随后生成的肌醇1,4,5-三磷酸酯（IP3），Ca2 +可能会从细胞内储存物中释放出来。假定神经元损伤导致ATP流出到细胞外空间，随后激活小胶质细胞。 ATP诱导的P2X-嘌呤受体过度去极化可通过向外整流钾离子通道和使非增殖性小胶质细胞中的P2Y-嘌呤受体超极化来抵消。

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