期刊
TRENDS IN NEUROSCIENCES
卷 40, 期 5, 页码 276-294出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2017.03.006
关键词
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资金
- National Institutes of Health (NIH)/National Institute of Neurological Disorders and Stroke (NINDS) [K08NS091248]
- Takeda Science Foundation
- Japan Health Foundation
- Ministry of Education, Science, Sports, Culture, and Technology [40450829, 15H05871]
- Simons Foundation
- March of Dimes
- NIH/National Institute of General Medical Sciences (NIGMS) [R21GM118944]
- NIH/National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) [R01DK093501]
- NIH/NINDS [5R01NS40109-14]
- Grants-in-Aid for Scientific Research [15H05871, 15K09611, 15K21731] Funding Source: KAKEN
Pharmacoresistant seizures and cytotoxic cerebral edema are serious complications of ischemic and traumatic brain injury. Intraneuronal Cl- concentration ([Cl-](i)) regulation impacts on both cell volume homeostasis and Cl--permeable GABA(A) receptor-dependent membrane excitability. Understanding the pleiotropic molecular determinants of neuronal [Cl-](i) - cytoplasmic impermeant anions, polyanionic extracellular matrix (ECM) glycoproteins, and plasmalemmal Cl- transporters - could help the identification of novel anticonvulsive and neuroprotective targets. The cation/Cl- cotransporters and ECM metalloproteinases may be particularly druggable targets for intervention. We establish here a paradigm that accounts for recent data regarding the complex regulatory mechanisms of neuronal [Cl-](i) and how these mechanisms impact on neuronal volume and excitability. We propose approaches to modulate [Cl-](i) that are relevant for two common clinical sequela of brain injury: edema and seizures.
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