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Neuronal differentiation modifies the effect of ethanol exposure on voltage-dependent calcium channels in NG 108-15 cells
Affiliation:1. Institute of Pharmacological Sciences, University of Milan, Milan, Italy;2. Department of Experimental Medicine and Biochemical Sciences, University of Rome “Tor Vergata,” Rome, Italy;3. Department of Pharmacology, School of Medicine, University of Milan, Milan, Italy;1. School of Information and Software Engineering, University of Electronic Science and Technology of China, Chengdu, 610054, China;2. Guangxi Colleges and Universities Key Laboratory of Cloud Computing and Complex Systems, Guilin University of Electronic Technology, Guilin 541004, China;1. Johns Hopkins University, Centre for Clinical Global Health Education (CCGHE), Baltimore, MD, USA
Abstract:
The effect of prolonged (72 h) ethanol (200 mM) exposure on the labeling of L-type (using tritiated PN 200-110) and N-type (using iodinated ω-conotoxin) voltage-dependent calcium channels was investigated in cultured NG 108-15 cells. In undifferentiated cells ethanol produced an 80% increase in PN 200-110 Bmax and no changes in ω-conotoxin binding. Differentiation had a profound effect on the response of cells to ethanol, which in differentiated neuron-like cells decreased w-conotoxin binding (−53.5%) leaving PN 200-110 labeling of L-type channels unaffected. The effect was time dependent and reversible upon ethanol withdrawal. The decreased ω-conotoxin binding was accompanied by a reduced ability of ω-conotoxin to inhibit K+-stimulated calcium uptake. The results demonstrate that in cultured NG 108-15 cells ethanol differentially affects DHP and ω-conotoxin-sensitive, voltage-dependent calcium channels and that the effect is also modulated by differentiation of the cell to a neuronal phenotype.
Keywords:
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