Regulation and effects of intracellular Cl concentrations

（1） Intraneuronal Cly D1= Iye D1 concentrations （[Cly D1= Iye D1]i） and immediately early gene （c-fos） expressionIntracerebroventricular administration of a Cly D1-Iye D1 pump inhibitor， ethacrynic acid， caused convulsions in mice。C-Fos的表达在混乱后60分钟和10-14天的高峰期被刺激了。神经增长因子的表现、GABA神经元的损害和确定可持续性的发展也是可见的。A transient increase in neuronal [Cly D1-y D1]i thus appeared to cause biphasic increases in c-fos expression and related modulation of neuronal functions。（2）ammonia-induced increases in neuronal [ClイイD1=イエD1]iA neurotoxic factor in hepatic encephalopathy， ammonia （2 mM， 48 hr）， increased [ClイイD1-イエD1]i in cultured rat hippocampal neurons。在蛋白激酶C激活的诱导下，发现了一种增强的离子交换剂表达（AE 3）。（3） ClイD1=イエD1 transport in hypoxia/reoxygenaion-induced changes in pHi and {CaイイD12+イエD1]i in myocytesUnder hypoxia/reoxygenaion conditions， pHi decreased and [CaイイD12+イエD1]i increased During hypoxia and reoxygenation， respectively。Inhibitors of anion exchanger （SITS and DIDS） and removal of medium Cl-D1或HCO-D23-D2 attenuated such changes in pHi and [Ca-D12+-D1]i.蛋白激酶C的抑制剂略微减少了pH值中的变化。Involvement of anion exchanger in hypoxia-induced pHi changes was first demonstrated with the resulting inhibitory effects on reoxygenation-induced increases in [Cai-D12 + Cai-D1]i.（4）神经ClyD 1 = ClyD 1泵新ClyD 1运输机、ClyD 1泵D1泵分离为520 kDa蛋白质复合体。SDS-PAGE分析显示了4个亚单位（51、55、60和62 kDa）和51 kDa的蛋白质出现在催化亚单位。一种55 kDa蛋白质的cDNA从大鼠脑cDNA库中克隆出来，其主要结构被认为是一种含有475氨基酸的新肽。

(1) Intraneuronal ClィイD1=ィエD1 concentrations ([ClィイD1=ィエD1]i) and immediately early gene (c-fos) expressionIntracerebroventricular administration of a ClィイD1-ィエD1 pump inhibitor, ethacrynic acid, caused convulsions in mice. Expression of c-fos was stimulated biphasically with the peaks at 60min and 10-14 days after the convulsion. Expression of nerve growth factor, damage of GABAergic neurons and development of seizure susceptibility were also observed. A transient increase in neuronal [ClィイD1-ィエD1]i thus appeared to cause biphasic increases in c-fos expression and related modulation of neuronal functions.(2) Mechanisms of ammonia-induced increases in neuronal [ClィイD1=ィエD1]iA neurotoxic factor in hepatic encephalopathy, ammonia (2 mM, 48 hr), increased [ClィイD1-ィエD1]i in cultured rat hippocampal neurons. The increase was found to be due to enhanced expression of anion exchanger (AE3) mediated by protein kinase C activation.(3) ClィイD1=ィエD1 transport in hypoxia/reoxygenaion-induced changes in pHi and {CaィイD12+ィエD1]i in myocytesUnder hypoxia/reoxygenaion conditions, pHi decreased and [CaィイD12+ィエD1]i increased during hypoxia and reoxygenation, respectively. Inhibitors of anion exchanger (SITS and DIDS) and removal of medium ClィイD1-ィエD1 or HCOィイD23ィエD2 attenuated such changes in pHi and [CaィイD12+ィエD1]i. Inhibitors of protein kinase C slightly reduced the changes in pHi. Involvement of anion exchanger in hypoxia-induced pHi changes was first demonstrated with the resulting inhibitory effects on reoxygenation-induced increases in [CaィイD12+ィエD1]i.(4) Subunits and cDNA cloning of neuronal ClィイD1=ィエD1 pumpA new ClィイD1-ィエD1 transporter, ClィイD1-ィエD1 pump, was isolated as 520 kDa protein complex from the rat brain. SDS-PAGE analyses yielded 4 subunits (51, 55, 60 and 62kDa), and 51kDa protein appeared to be a catalytic subunit. cDNA for 55 kDa protein was cloned from the rat brain cDNA library, and its primary structure was assumed to be a new peptide with 475 amino acids.