چاپ صفحه |  صفحه نخست سامانه |  چکیده مقاله |  نویسندگان |  دانلود مقاله | دانشگاه علوم پزشکی تبریز |
| Agonists of a7 nicotinic acetylcholine receptors (nAChRs) are currently being considered as therapeutic approaches for managing cognitive deficits in Alzheimer’s disease (AD). Present study was designed to evaluate the effect of a7 nAChR selective activation by PHA-543613 (PHA) on beta-amyloid (Ab)25–35-mediated cognitive deficits in mice. For this purpose, PHA (1 mg/kg, i.p.), a selective a7 nAChR agonist, and galantamine (Gal) (3 mg/kg, s.c.), an acetylcholine-esterase inhibitor (AChEI) effects on a7 nAChR were tested in Ab25–35-received (intracerebroventricular, 10 nmol) mice model of AD. Methyllycaconitine (MLA) (1 mg/kg, i.p.), a a7 nAChR antagonist, was used for receptor blockage effects evaluation. Working and reference memory in animals was assessed by the Morris water maze (MWM) task. The mRNA and protein levels of a7 subunit were analyzed by real-time PCR and Western blotting, respectively. PHA and Gal, ameliorate Ab-impaired working and reference memory. However, Gal had less effect than PHA in this regard. Pretreatment with MLA reverses both Gal and PHA effects in MWM. PHA and Gal treatment prevent Ab-induced a7 subunit protein reduction, but Gal has lesser effect than PHA. This effect blocked by pretreatment with MLA. In neither the pretreatment nor treatment group, the mRNA levels of nAChR a7 subunit were significantly changed. Therefore, a7 nAChR activation, reduces Ab-induced cognitive deficits and increasesthea7 protein level and subsequent neuron survival. However, blockage of receptor, increases Ab toxicity and cognitive impairment and reduces the a7 nAChR protein level and flowing neuroprotection. |
| نویسنده | نفر چندم مقاله |
|---|---|
| سعید صدیق اعتقاد | اول |
| مهناز طالبی | دوم |
| جواد محمودی | سوم |
| شیرین ببری | چهارم |
| داریوش شانه بندی | پنجم |
| نام فایل | تاریخ درج فایل | اندازه فایل | دانلود |
|---|---|---|---|
| 1-s2.0-S0306452215003486-main.pdf | 1397/07/14 | 1172363 | دانلود |
