Expression of STIM1 in brain and puncta-like co-localization of STIM1 and ORAI1 upon depletion of Ca²⁺ store in neurons

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• 作者：Monika E. Klejman ; Joanna Gruszczynska-Biegala ; Anna Skibinska-Kijek ; Marta B. Wisniewska ; Katarzyna Misztal ; Magdalena Blazejczyk ; Lukasz Bojarski ; Jacek Kuznicki
• 关键词：SOCE ; STIM ; ORAI ; Capacitative Ca²⁺ entry ; Neurons ; Brain ; Endoplasmic reticulum
• 刊名：Neurochemistry International
• 出版年：2009
• 出版时间：January 2009
• 年：2009
• 卷：54
• 期：1
• 页码：49-55
• 全文大小：1064 K

文摘

Recent findings indicate that Store Operated Ca²⁺ Entry (SOCE) in non-excitable cells is based on the interaction of ER calcium sensor STIM1 with the plasma membrane Ca²⁺ channel protein ORAI1. However, despite physiological evidence for functional SOCE in neurons, its mechanism is not known. Using PCR, immunoblotting and immunohistochemical methods we show that STIM1 protein is present in the mouse brain. The protein and mRNA levels of STIM1 are similar in the thalamus, the hippocampus, the cortex and the amygdala and the higher level is observed in the cerebellum. Immunohistochemistry of the cortex and the hippocampus of brain sections shows that STIM1 is present in cell bodies and dendrites of pyramidal neurons. In the cerebellum STIM1 is present in Purkinje and granule cells. The same immunostaining pattern is observed in cultured hippocampal and cortical neurons. Localization of YFP-STIM1 and ORAI1 changes from a dispersed pattern in untreated cortical neurons to puncta-like pattern in cells with a Ca²⁺ store depleted by thapsigargin treatment. The YFP-STIM1(D76A) dominant positive mutant, which is active regardless of the Ca²⁺ level in ER, concentrates as puncta even without depletion of the neuronal Ca²⁺ store. Also, this mutant forces ORAI1 redistribution to form puncta-like staining. We suggest that in neurons, just as in non-excitable cells, the STIM1 and ORAI1 proteins are involved in SOCE.