Department of Anatomy and Cell Biology, Yamagata University School of Medicine, Iida-nishi 2-2-2, Yamagata 990-9585, Japan.
Neurosci Lett. 2011 May 2;494(3):185-9. doi: 10.1016/j.neulet.2011.02.062. Epub 2011 Mar 6.
Diacylglycerol kinase (DGK), which consists of several isozymes, plays a pivotal role in lipid second-messenger diacylglycerol metabolism. A nuclear isozyme, DGKζ, which is translocated from the nucleus to the cytoplasm in hippocampal neurons under transient ischemic stress, is implicated in nuclear events of delayed neuronal death. Kainate (KA)-induced seizure is another model used to study excitotoxic stress. Therefore, we examined whether DGKζ is implicated in a different type of degenerative excitotoxicity in hippocampal neurons. We conducted immunohistochemical analysis of rat hippocampi after KA-induced seizures. DGKζ in hippocampal neurons shuttles from the nucleus to the cytoplasm. It never relocates to the nucleus during KA-induced seizures. Marked change in the immunoreactivity is first observed in CA1 pyramidal neurons 2h after injection during stage 3 seizures. Immunoreactivity for DGKι remains unchanged in the cytoplasm. That for NeuN remains mostly unchanged in the nucleus. Results show that nucleocytoplasmic translocation of DGKζ also occurs in a different model of excitotoxicity that results in apoptotic neuronal death. Cytoplasmic translocation of DGKζ might be involved in early events of the apoptotic cell death pathway in hippocampal neurons under stressed conditions.
二酰基甘油激酶（DGK）由几种同工酶组成，在脂质第二信使二酰基甘油代谢中起着关键作用。一种核同工酶，DGKζ，在短暂性缺血应激下从海马神经元的核内易位到细胞质，与迟发性神经元死亡的核内事件有关。红藻氨酸（KA）诱导的癫痫发作是另一种用于研究兴奋性毒性应激的模型。因此，我们研究了 DGKζ 是否参与海马神经元中不同类型的退行性兴奋性毒性。我们对 KA 诱导的癫痫发作后的大鼠海马进行了免疫组织化学分析。DGKζ 在海马神经元中从核内易位到细胞质。在 KA 诱导的癫痫发作期间，它从未重新定位到核内。在 3 期癫痫发作期间注射后 2 小时，首先在 CA1 锥体神经元中观察到免疫反应性的明显变化。DGKι 的免疫反应性在细胞质中保持不变。NeuN 的免疫反应性在核内基本保持不变。结果表明，DGKζ 的核质易位也发生在导致凋亡性神经元死亡的另一种兴奋性毒性模型中。在应激条件下，DGKζ 的细胞质易位可能参与海马神经元中凋亡性细胞死亡途径的早期事件。
