SHSY5Y اثر آگونيست ها و آنتاگونيست هاي گيرنده هاي نيكوتيني استيل كولين بربيان آنزيم استيل كولين استراز در سلول هاي

Effect of Nicotinic Receptors Agonist and Antagonist on acetylcoline sterase Exprition in SHSYSY Cells

Objective: The aim of the present study was to examine the mechanism by which Beta-amyloid interact with nicotinic receptors and changes the level of acetyfcholinesterase (AChE) in Alzheimerʹs disease. Materials and Methods: SHSY5Y and PCI2 human ncuroblastoma and pheochromocytonia cells were cultured and effects of ABeta, and nicotinic receptor agonists and antagonists were investigated. Results: ABeta1_.42 significantly increased AChE in SHSYSY cells. The effect of ABeta was blocked by nicotine and a-bungarotoxin (Alpha-Bgt) a selective antagonist of a7 nicotinic acetylcholine receptor (nAChR). Nicotine alone had no effect on AChH activity. but acetylcholine, choline and carbamoylcholine all increased ACNE activity in these cells. Nicotinic receptor antagonists such as Alpha-Bgt., methellycaconitine (MLA), mecamylamine and dihydro Beta -crythroidin (DIVE) did not have any effect on AChE activity. In contrast. selective a7 nAChR antagonistʹs Alpha-Bgt and MLA in concomitant with 10miuM nicotine, significantly increased AChE activity in SHSY5Y cells, but non- Alpha7 preferring antagonist, DHBetaE was not effective. This activation was not seen in PC 12 cells. Acetylcholine (but not nicotine) increased Alpha7 nAChR density in SHSYSY cell membrane. Conclusion: These results demonstrate that increase in ACNE activity in these cells is due to Alpha7 nAChR.