Corticosterone affects the differentiation of a neuronal cerebral cortex-derived cell line through modulation of the nicotinic acetylcholine receptor

• Published in: Neuroscience 2014-08, Vol.274, p.369-382
• Main Authors: Baier, C.J, Franco, D.L, Gallegos, C.E, Mongiat, L.A, Dionisio, L, Bouzat, C, Caviedes, P, Barrantes, F.J
• Format: Article
• Language: English
• Subjects: Aconitine - analogs & derivatives; Aconitine - pharmacology; Animals; cell cycle; Cell Cycle - drug effects; Cell Cycle - physiology; Cell Line; Cell Membrane - drug effects; Cell Membrane - physiology; Cell Proliferation - drug effects; Cell Proliferation - physiology; Cerebral Cortex - drug effects; Cerebral Cortex - physiology; Corticosterone - metabolism; glucocorticoids; ion channel; Mice; Neurogenesis - drug effects; Neurogenesis - physiology; Neurology; Neurons - drug effects; Neurons - physiology; nicotine; Nicotine - pharmacology; Nicotinic Agonists - pharmacology; Nicotinic Antagonists - pharmacology; Patch-Clamp Techniques; Receptors, Nicotinic - genetics; Receptors, Nicotinic - metabolism; stress
• ISSN: 0306-4522; 1873-7544
• DOI: 10.1016/j.neuroscience.2014.05.049

Highlights • Chronic corticosterone (CORT) treatment impairs the differentiation of a neuronal cell line, CNh. • CORT hinders the G0/G1 arrest of CNh cells, promoting their proliferation. • CORT impairs the expression and functionality of nicotinic acetylcholine receptors (AChRs). • Overexpression of GFP-labeled α7-AChR restores the cell cycle affected by CORT. • AChRs signaling is involved in the progression of the cell cycle in CNh cells.