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脉络丛离子转运体表达与脑脊液分泌

Choroid plexus ion transporter expression and cerebrospinal fluid secretion.

作者信息

Keep R F, Xiang J, Ulanski L J, Brosius F C, Betz A L

机构信息

Department of Surgery (Neurosurgery), University of Michigan, Ann Arbor, USA.

出版信息

Acta Neurochir Suppl. 1997;70:279-81. doi: 10.1007/978-3-7091-6837-0_86.

DOI:10.1007/978-3-7091-6837-0_86
PMID:9416346
Abstract

The Cl-/HCO3- exchanger (AE2 isoform) and the Na+/K(+)-ATPase at the choroid plexus are both thought to be involved in CSF secretion. However, both transport mechanisms are also postulated to have a role in CSF ion homeostasis raising questions as to which parameters control the expression of these transporters? Northern blots have been used to assess AE2 mRNA levels in rats subjected to alterations in blood pH or blood osmolality (a factor affecting CSF secretion). Six hours of alkalosis induced a 40% increase in AE2 mRNA (p < 0.01), suggesting that alterations in the expression of this transporter play a role in CSF pH homeostasis. In contrast, changes in osmolality did not affect AE2 mRNA. Western blots of Na+/K(+)-ATPase subunits were also examined to determine whether hypo and hyperkalemia affect protein levels of this transporter. There was a positive correlation between the plasma K+ concentration and both alpha 1- and beta 1 subunit protein levels suggesting a role for this transporter in CSF K+ homeostasis. As changes in plasma K+ and pH affect choroid plexus ion transporters but do not appear to alter CSF production, these results suggest the presence of compensatory mechanisms. Understanding of such mechanisms may facilitate therapeutic control of CSF production.

摘要

脉络丛中的Cl⁻/HCO₃⁻交换体(AE2亚型)和Na⁺/K⁺-ATP酶都被认为参与脑脊液分泌。然而,这两种转运机制也被假定在脑脊液离子稳态中起作用,这就引发了关于哪些参数控制这些转运体表达的问题。Northern印迹法已被用于评估血液pH值或血液渗透压(影响脑脊液分泌的一个因素)发生改变的大鼠中AE2 mRNA水平。碱中毒6小时导致AE2 mRNA增加40%(p < 0.01),这表明该转运体表达的改变在脑脊液pH稳态中起作用。相比之下,渗透压的变化并不影响AE2 mRNA。还检测了Na⁺/K⁺-ATP酶亚基的Western印迹,以确定低钾血症和高钾血症是否影响该转运体的蛋白质水平。血浆K⁺浓度与α1和β1亚基蛋白质水平之间呈正相关,表明该转运体在脑脊液K⁺稳态中起作用。由于血浆K⁺和pH的变化影响脉络丛离子转运体,但似乎不会改变脑脊液生成,这些结果提示存在代偿机制。对这些机制的理解可能有助于脑脊液生成的治疗控制。

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