کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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1938103 | 1050732 | 2007 | 6 صفحه PDF | دانلود رایگان |
Corticotrophin-releasing factor (CRF) is the main regulator of the body’s stress axis and its signal is translated through G-protein-coupled CRF receptors (CRF-R1, CRF-R2). Even though CRF receptors are present in the midbrain dopamine neurons, the cellular mechanism of CRF action is not clear yet. Since voltage-dependent Ca2+ channels are highly expressed and important in dopamine neuronal functions, we tested the effect of CRF on voltage-dependent Ca2+ channels in MN9D cells, a model of dopamine neurons. The application of CRF-related peptide, urocortin 1, reversibly inhibited T-type Ca2+ currents, which was a major Ca2+ channel in the cells. The effect of urocortin was abolished by specific CRF-R1 antagonist and was mimicked by protein kinase C (PKC) activator, phorbol 12-myristate 13-acetate. PKC inhibitors abolished the effect of urocortin. These results suggest that urocortin modulates T-type Ca2+ channel by interacting with CRF-R1 via the activation of PKC signal pathway in MN9D cells.
Journal: Biochemical and Biophysical Research Communications - Volume 358, Issue 3, 6 July 2007, Pages 796–801