The enhancement effects of amyloid β protein on in vivo hippocampal long term depression in rats

Abstract

Objective To investigate the exact protocol eliciting the hippocampal CA1 long-term depression (LTD) of rats in vivo and the effect of amyloid β-protein (Aβ) on the LTD. Method By applying test stimulation to Schaffer collateral in hippocampal CA1 region in rats, recorded the in vivo field excitatory postsynaptic potentials (fEPSPs); further, observed the induction of LTD with different low frequency stimulation (LFS) and investigated the effect of Aβ25-35 on the LTD. Results Prolonged LFS (1, 5 and 10 Hz) but not paired-pulse stimulus (PPS) effectively elicited the LTD in the hippocampal CA1 region, with significantly decreased amplitude of fEPSPs after LFS; 1 Hz 900 pulses group induced a stronger LTD, being (63.7±3.8)% at 120 min post-LFS, lower (P 0.05); after applying 12.5 nmol and 25 nmol Aβ25-35, the amplitude of fEPSPs decreased to (63.2±3.8)% and (46.8±3.9)%, respectively, and lower and than that in control ((73.9±3.0)%, P<0.05). Conclusion Prolonged LFS effectively induced in vivo hippocampal LTD of rats, which provides an important electrophysiological protocol for the study of synaptic plasticity; Aβ25-35 injection don't affect the baseline synaptic transmission, but dose-dependently enhance the in vivo hippocampal LTD of rats, indicating that Aβ-induced LTD facilitation may be involved the early impairment of learning and memory in Alzheimer's disease. Key words: Long-term depression; Amyloid β protein; Hippocampus; Alzheimer's disease