CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine-induced status epilepticus
CCR7, CCR8, CCR9 and CCR10 in the mouse hippocampal CA1 area and the dentate gyrus during and after pilocarpine-induced status epilepticus
复制标题
DOI：
10.1111/j.1471-4159.2006.04272.x
复制
发表时间：
2007-02-01
影响因子：
4.7
通讯作者：
Tang, Feng Ru
中科院分区：
文献类型：
--
作者：
Liu, Jian Xin;Cao, Xia;Tang, Feng Ru
本研究从蛋白和mRNA水平显示了正常瑞士小鼠海马中的CCR 7、CCR 8、CCR 9和CCR 10。CCR 7、CCR 9和CCR 10主要定位于海马主细胞和部分中间神经元。CCR 9也被发现在苔藓纤维和/或终端，提示轴突或突触前定位，和CCR 10在CA 1区锥体神经元的顶端树突。在中间神经元中观察到CCR 8。双标记免疫细胞化学显示，大多数的钙结合蛋白（CB）-，钙视网膜蛋白（CR）-和小清蛋白（PV）-免疫阳性神经元表达CCR 7 -10，除了CR-免疫阳性细胞，其中只有10 - 12%表达CCR 8。在匹罗卡品诱导的癫痫持续状态期间和之后，CCR 7、CCR 8、CCR 9和CCR 10蛋白在不同时间点以不同模式发生进行性变化。灵敏的实时荧光定量PCR在mRNA水平上显示了相似的变化模式。在慢性阶段，即毛果芸香碱诱导癫痫持续状态后2个月，CB、CR和PV免疫阳性中间神经元中CCR 7 -10表达的显着减少可能表明存活中间神经元的表型变化。慢性期CCR 7、CCR 8和CCR 9与胶质细胞酸性蛋白（GFAP）的双标记可能表明反应性星形胶质细胞中的诱导表达。因此，本研究可能首次提供证据表明CCR 7 -10可能参与正常海马活动。CCR 7 -10在癫痫持续状态中和癫痫持续状态后的进行性变化可能为揭示癫痫持续状态后神经元丢失和癫痫发生机制开辟了新的领域。
The present study showed CCR7, CCR8, CCR9 and CCR10 in the normal Swiss mouse hippocampus at both protein and mRNA levels. CCR7, CCR9 and CCR10 were mainly localized in hippocampal principal cells and some interneurons. CCR9 was also found in the mossy fibres and/or terminals, suggesting an axonal or presynaptic localization, and CCR10 in apical dendrites of pyramidal neurons in the CA1 area. CCR8 was observed in interneurons. Double-labelling immunocytochemistry revealed that most of calbindin (CB)-, calretinin (CR)- and parvalbumin (PV)-immunopositive neurons expressed CCR7-10, except CR-immunopositive cells in which only 10 to 12% expressed CCR8. During and after pilocarpine-induced status epilepticus, progressive changes of each of CCR7, CCR8, CCR9 and CCR10 proteins occurred in different patterns at various time points. Sensitive real-time PCR showed similar change patterns at mRNA level. At the chronic stage, i.e. at 2 months after pilocarpine-induced status epilepticus, significant reduction of CCR7-10 expression in CB-, CR- and PV-immunpositive interneurons may suggest the phenotype change of surviving interneurons. Double labelling of CCR7, CCR8 and CCR9 with glial fibrillary acidic protein (GFAP) at the chronic stage may suggest an induced expression in reactive astrocytes. The present study may, therefore, for the first time, provide evidence that CCR7-10 may be involved in normal hippocampal activity. The demonstration of the progressive changes of CCR7-10 during and after status epilepticus may open a new area to reveal the mechanism of neuronal loss after status epilepticus and of epileptogenesis.