Molecular mechanisms of cerebrospinal fluid production.

Molecular mechanisms of cerebrospinal fluid production.
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DOI:
10.1016/j.neuroscience.2004.07.003
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发表时间:
2004
期刊:
影响因子:
3.3
通讯作者:
Millar, ID
Millar, ID
中科院分区:
医学3区
文献类型:
--
作者:
Brown, PD;Davies, SL;Seake, T;Millar, ID

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脉络丛上皮细胞分泌脑脊液(CSF),这一过程涉及到Na+、Cl-和HCO3-从血液到脑室的运输。离子的单向转运是由于上皮细胞的极性,即面向血液的(基侧)膜上的离子转运蛋白与心室(心尖)膜上的离子转运蛋白不同。离子的运动产生渗透梯度,从而驱动H2 O的分泌。许多方法(如同位素通量研究、电生理、RT-PCR、原位杂交和免疫细胞化学)已被用来确定脉络丛上皮中离子转运体和通道的表达。这些转运蛋白中的大多数现在已经定位于特定的膜上。例如,Na~+-K~+-ATPase、K~+通道和Na~+-2Cl~-K~+共转运蛋白在顶膜表达。相比之下,基侧膜含有Cl--HCO3-交换器、各种Na+偶联HCO3-转运体和K+-Cl3-共转运体。水通道蛋白1介导水在根尖膜上的转运,但穿过基底膜的途径尚不清楚。一个哺乳动物脉络丛分泌脑脊液的模型被提出,以适应这些蛋白质。该模型还解释了K+从脑脊液运输到血液的机制。
The epithelial cells of the choroid plexuses secrete cerebrospinal fluid (CSF), by a process which involves the transport of Na+, Cl- and HCO3- from the blood to the ventricles of the brain. The unidirectional transport of ions is achieved due to the polarity of the epithelium, i.e. the ion transport proteins in the blood-facing (basolateral) membrane are different to those in the ventricular (apical) membrane. The movement of ions creates an osmotic gradient which drives the secretion of H2 O. A variety of methods (e.g. isotope flux studies, electrophysiological, RT-PCR, in situ hybridization and immunocytochemistry) have been used to determine the expression of ion transporters and channels in the choroid plexus epithelium. Most of these transporters have now been localized to specific membranes. For example, Na+-K+ ATPase, K+ channels and Na+-2Cl--K+ cotransporters are expressed in the apical membrane. By contrast the basolateral membrane contains Cl--HCO3 exchangers, a variety of Na+ coupled HCO3- transporters and K+-Cl- cotransporters. Aquaporin 1 mediates water transport at the apical membrane, but the route across the basolateral membrane is unknown. A model of CSF secretion by the mammalian choroid plexus is proposed which accommodates these proteins. The model also explains the mechanisms by which K+ is transported from the CSF to the blood.
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发表时间: 2000-06-01
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