LONG TERM POTENTIATION IN THE MODEDL OF ALZHEIMER'S DISEASE
Uzakov Sh.S., Markevich V.A.
Institute of higher nervous activity and neurophysiology Russian Academy of Sciences, Moscow, Russia. email@example.com Amyloid Abeta plays the key part in Alzheimer's disease (AD). It was shown that memory deficits, observed during AD is correlated with depression of LTP induction in hippocampus. This effect was previously examined in СА1 field. It was found that injection of Abeta (25-35) decrease LTP via concentration-dependent manner. The subsequent accumulation of Aβ leads the loss of cholinergic neurones in medial septum. Expression of nerve growth factor (NGF) in medial septum partially prevents the loss of cholinergic neurons and compensates the effect of Abeta (25-35). The aim of our work was to check the hypothesis that the over expression of NGF can compensate the influence of Abeta (25-35) on LTP induction in dentate gyrus (DG). In acute experiments on Wistar rats it was shown that Abeta (25-35) disrupted the induction and maintenance of LTP in DG and this effect depended on amyloid amount. Injection of Aβ(35–25) had no significant effect on LTP compared with control group. Preliminary application of a lentivirus suspension of pCaKMII-NGF-GFP into DG in 12-14 days prior to experiment provided over expression of NGF and compensated the effect of Abeta (25-35). This confirms the put-forward hypothesis.
ВЛИЯНИЕ ПРОЛИЛ–ГЛИЦИЛ–ПРОЛИНА (PGP) НА УРОВЕНЬ КАЛЬЦИЯ В ЦИТОПЛАЗМЕ ТУЧНЫХ КЛЕТОК ПРИ ИХ АКТИВАЦИИ ВЕЩЕСТВАМИ РАЗЛИЧНОЙ ПРИРОДЫ