Aims: 

It is known that a fragment of amyloid protein, Ab_1-42, is lethal to hippocampal cells, producing recent memory deficits characteristic of Alzheimer's disease (AD). Dysfunction in calcium homeostasis is one of the events in the pathogenesis of AD. The aim of the study was to discover changes in calcium signaling in hippocampal cells with experimental induced AD.

Methods: 

The changes in neuronal Ca²⁺homeostasis were studied on rat hippocampal cell culture in control condition and under one-day b-amyloid-induced modification. The cytoplasmic free Ca²⁺concentration ([Ca²⁺]_i) was measured using fura-2 based microfluorometry.

Results: 

The recovery of depolarization-induced [Ca²⁺]_i increase was delayed on 200 s in amyloid-treated neurons compared with recovery at control conditions. Basal [Ca²⁺]_i in cells exposed to b-amyloid was higher on 67 ± 9 nM (mean SD, P < 0.05) than that in control cells. The amplitude of depolarization-induced [Ca²⁺]_i increase in amyloid-treated neurons was lower on 189 ± 26 nM (P < 0.05) than depolarization-induced [Ca²⁺]_i increase in control cells. The morphology of neurons has been changed essentially by influence of b-amyloid.

Conclusion: 

These results demonstrated strong b-amyloid affect on hippocampal cell culture. Smaller response of the b-amyloid-treated cells to depolarization compared with that in control condition could be explained by action of Ab_1-42 on voltage-gated calcium channels. Longer after-depolarization recovery period and higher resting Ca²⁺level peculiar to b-amyloid-modificated cells might be related with damaging of Ca²⁺extrusion mechanisms. We conclude that b-amyloid causes a strong toxic effect on hippocampal cell culture by changing Ca²⁺signaling in it.