Volume activated anion channel and astrocytic cellular edema in traumatic brain injury and stroke.
Volume activated anion channel and astrocytic cellular edema in traumatic brain injury and stroke.
复制标题
创伤性脑损伤和中风中的容量激活阴离子通道和星形胶质细胞水肿。
DOI：
10.1007/0-387-23752-6_15
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发表时间：
2004
影响因子：
--
通讯作者：
Kimelberg,HaroldK
中科院分区：
文献类型：
--
作者：
Kimelberg,HaroldK
A number of pathological states are associated with inappropriate channel activities, eg, dysfunction of chloride channels in kidney diseases, cystic fibrosis and myotonias, 1 and the Gardos potassium channel in sickle cell anemia. 2 Also a number of other CNS diseases such as epilepsy and cerebral ischemia are thought to be associated with ion channel dysfunction. 3 However, there has been no evidence as yet for the dysfunction of the volume regulated anion (VRAC) channel, also known as volume sensitive organic osmolyte anion channels (VSOAC) and, when monitored electrophysiologically, as ICl, swell. Other acronyms are VSOR (volume sensing outwardly rectifying Cl-channel) and VRClC (volume regulated chloride channel). 4 These channels are currently known only by their electrophysiological and transport activities, and in spite of several claims, their molecular basis or bases are not known with any certainty. However, their physiology is definitive and there have been no pathological states clearly associated with that. 5, 6 Their molecular identification would, of course, make association of VRACs with pathologies easier, as it would allow manipulation of its expression and the identification of more specific inhibitors than are available to date. The main functions of VRACs are thought to be volume regulation, ion secretion and cell proliferation. In volume regulation, they are activated when cells are swollen rapidly, as when experimentally exposed to a rapid decrease in medium osmolarity. 5, 7 They are also activated when the media osmolarity is gradually reduced as measured by release of taurine and D-aspartate but with no detectable change in relative cell volume, a process termed isovolumetric regulation. 8 Presumably, this results in activation of VRACs with a time course coincident with the rate of the osmolarity change, and the sensitivity to the volume increase is such that the amount of swelling minimally required to activate is
