Kim Myeung Ju, Chung Yoon Hee, Joo Kyeung Min, Oh Goo Taeg, Kim Jaewoo, Lee Bonghee, Cha Choong Ik
Department of Anatomy, Cheju National University College of Medicine, 1 Ara 1-Dong, Jeju-Si, Jeju-Do 690-756, South Korea.
Neurosci Lett. 2004 Oct 7;369(1):39-43. doi: 10.1016/j.neulet.2004.07.047.
Nitric oxide (NO) participates in synaptic plasticity, neuronal development, and apoptosis. The involvement of NO and ionic calcium in synaptic plasticity imply that NO may exert an effect on Ca2+ channels. Therefore, we investigated changes in the expressions of calcium channel subunits (Cav1.2/alpha1C, Cav1.3/alpha(1D), Cav2.1/alpha1A, and Cav2.2/alpha1B) in nNOS knock-out (-/-) (nNOS((-/-))) mouse cerebellum using an immunohistochemical approach. We found that the immunoreactivities of the Cav1.2 and Cav1.3 subunits were reduced in the cell bodies of Purkinje cells in these mice and that the signal of the Cav1.2 subunit in neurons and of the Cav1.3 subunit in the neuropils of nNOS((-/-)) mice cerebellar nuclei were significantly down-regulated. We show, for the first time, that prolonged NO deficiency in the cerebellum may affect calcium channel protein expressions, especially, of the Cav1.2 and Cav1.3 subunits.
一氧化氮(NO)参与突触可塑性、神经元发育和细胞凋亡。NO和离子钙参与突触可塑性表明NO可能对Ca2+通道产生影响。因此,我们采用免疫组织化学方法研究了nNOS基因敲除(-/-)(nNOS(-/-))小鼠小脑钙通道亚基(Cav1.2/α1C、Cav1.3/α1D、Cav2.1/α1A和Cav2.2/α1B)表达的变化。我们发现,这些小鼠浦肯野细胞胞体中Cav1.2和Cav1.3亚基的免疫反应性降低,并且nNOS(-/-)小鼠小脑核神经元中Cav1.2亚基和神经毡中Cav1.3亚基的信号显著下调。我们首次表明,小脑中长期缺乏NO可能影响钙通道蛋白的表达,尤其是Cav1.2和Cav1.3亚基的表达。