Neurochemical and morphological studies on differentiation of NG108-15 cells by phorbol ester and forskolin |
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| Institution: | 1. Optics Laboratory, Applied Physics Department, The Maharaja Sayajirao University of Baroda, 390001, India;2. Centre for Sensors, Instrumentation and Cyberphysical System Engineering, IIT Delhi, 110016, India;3. Department of Electrical Engineering, University of Connecticut, Storrs, CT, 06269-4157, USA;4. Institute of Interdisciplinary Studies, The Maharaja Sayajirao University of Baroda, Vadodara, India;1. Malaysian Institute of Pharmaceuticals & Nutraceuticals, NIBM, Ministry of Science, Technology & Innovation (MOSTI), Pulau Pinang, Malaysia;2. Clinical Research Center, Hospital Seberang Jaya, Kementerian Kesihatan Malaysia, Pulau Pinang, Malaysia;3. Institute of Physiology, University of Wurzburg, Wurzburg, Germany;4. Atta-ur-Rahman Institute for Natural Product Discovery, Universiti Teknologi MARA (UiTM), Selangor Darul Ehsan, Malaysia;5. Pharmaceutical Design & Simulation (PhDS) Laboratory, School of Pharmaceutical Sciences, Universiti Sains Malaysia, Pulau Pinang, Malaysia;6. Advanced Medical and Dental Institute, Universiti Sains Malaysia, Pulau Pinang, Malaysia |
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| Abstract: | 12-O-tetradecanoylphorbol 13-acetate (TPA), forskolin or dibutyryl cAMP induced neurite outgrowth and inhibition of cell growth in NG108-15 cells. TPA, forskolin and dibutyryl cAMP significantly increased specific activity of choline acetyltransferase. Forskolin markedly stimulated cAMP accumulation, but not TPA, suggesting that forskolin could induce differentiation by increasing the cAMP content via adenylate cyclase activation, but TPA-induced differentiation seems not to be due to the raise of the cAMP level. Incubation of the cells with TPA, forskolin or dibutyryl cAMP for 24 h resulted in enhancement of 50 mM K+-evoked Ca2+ influx and neurite elongation, although incubation with these agents for 1 h didn't affect these events. From these results, it is suggested that TPA and forskolin induce differentiation of NG108-15 cells to acetylcholine neurons via different mechanisms: protein kinase C activation by TPA and cAMP-dependent protein kinase activation by forskolin. In addition, it is likely that Ca2+ channels in cells differentiated by TPA, forskolin or dibutyryl cAMP become sensitive to depolarization. |
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