Cav1.2, Cav1.3, and Cav2.1 in the mouse hippocampus during and after pilocarpine‐induced status epilepticus

Cav1.2, Cav1.3, and Cav2.1 in the mouse hippocampus during and after pilocarpine‐induced status epilepticus
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DOI:
10.1002/hipo.20263
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发表时间:
2007-03
期刊:
影响因子:
3.5
通讯作者:
Jie-hua Xu;L. Long;Y. Tang;Hai-tao Hu;F. Tang
Jie-hua Xu;L. Long;Y. Tang;Hai-tao Hu;F. Tang
中科院分区:
医学3区
文献类型:
--
作者:
Jie-hua Xu;L. Long;Y. Tang;Hai-tao Hu;F. Tang

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众所周知,钙结合蛋白在不同海马间神经元群中表达;然而,电压依赖性钙通道(Cav)是否也位于这些神经元中,在癫痫持续状态(SE)期间和之后发生改变,并参与癫痫活动尚未报道。在本研究中,我们发现三种电压门控钙通道亚型(Cav1.2、Cav1.3或Cav2.1)与不同的钙结合蛋白(钙结合蛋白(CB)、钙降钙蛋白(CR)和小白蛋白(PV))共定位。在匹罗卡品诱导的癫痫持续状态(PISE)期间和之后的早期阶段,在不同组的海马神经元中发现Cav1.2、Cav1.3 (L型)和Cav2.1 (P/Q型)的表达发生了显著变化。在PISE后1周和2个月,在反应性星形胶质细胞中诱导表达Cav1.3或Cav2.1。后一个时间点,胶质细胞CA1区PV与Cav1.2、CB、PV与Cav1.3或Cav2.1共定位比例较高,CR与Cav1.3或Cav2.1免疫阳性神经元共定位比例较低。因此,我们得出结论,电压门控钙通道在小鼠海马中间神经元的不同组中表达。在PISE期间和之后的急性期,CA1区不同功能组间神经元Cav1.2、Cav1.3或Cav2.1的上调或下调可能与其可塑性的变化有关。颗粒细胞中Cav1.2、Cav1.3或Cav2.1的上调可能与SE的发生直接相关。在PISE后1周和2个月,反应性星形胶质细胞中诱导Cav1.3或Cav2.1的表达表明,反应性星形胶质细胞中Cav1.3或Cav2.1相关的钙信号可能参与了癫痫发作活动的开始、维持或扩散。在慢性期(即PISE后2个月)的胶质细胞CA1区,PV和Cav1.2、CB或PV和Cav1.3或Cav2.1共定位的比例较高,CR和Cav1.3或Cav2.1免疫阳性神经元的比例较低,可能表明这种共定位可能与特定海马神经元群的存活或丧失有关。©2007 Wiley‐Liss, Inc。
Calcium binding proteins are well known to be expressed by different groups of hippocampal interneurons; however, whether voltage‐dependent calcium channels (Cav) are also localized in these neurons, changed during and after status epilepticus (SE), and involved in epileptic activity have not been reported. In the present study, we showed the colocalization of three subtypes of voltage‐gated calcium channels (Cav1.2, Cav1.3, or Cav2.1) with different calcium binding proteins such as calbindin (CB), calretinin (CR), and parvalbumin (PV). At early stages during and after pilocarpine‐induced status epilepticus (PISE), significant changes of expression of Cav1.2, Cav1.3 (L‐type), and Cav2.1 (P/Q‐type) were found in different groups of hippocampal neurons. Induced expression of Cav1.3 or Cav2.1 in reactive astrocytes was shown at 1 week and 2 months after PISE. At the latter time point, higher percentages of colocalization of PV and Cav1.2, CB, or PV and Cav1.3 or Cav2.1, lower percentages of CR and Cav1.3 or Cav2.1 immunoposivie neurons were observed in gliotic CA1 area. We therefore conclude that voltage‐gated calcium channels are expressed by different groups of hippocampal interneurons in the mouse. At acute stages during and after PISE, up‐ or down‐regulation of Cav1.2, Cav1.3, or Cav2.1 in functionally different groups of interneurons in CA1 area may be related to the changes of their plasticity. Up‐regulation of Cav1.2, Cav1.3, or Cav2.1 in granule cells may be directly related to the occurrence of SE. The induced expression of Cav1.3 or Cav2.1 in reactive astrocytes at 1 week and 2 months after PISE suggests that Cav1.3 or Cav2.1‐related calcium signaling in reactive astrocytes may be involved in initiation, maintenance or spread of seizure activity. In gliotic CA1 area at chronic stage (i.e., 2 months after PISE), the occurrence of higher percentages of colocalization of PV and Cav1.2, CB, or PV and Cav1.3 or Cav2.1, lower percentages of CR and Cav1.3 or Cav2.1 immunopositive neurons may suggest that such colocalizations may be linked to the survival or loss of particular group of hippocampal neurons. © 2007 Wiley‐Liss, Inc.