Induction of a rat model of Alzheimer's disease by amyloid-β did not change short term synaptic plasticity in CA1 area of hippocampus

Alzheimer’s disease (AD) has been suggested to be a form of neuroplasticity failure. In addition to long term maladaptive changes in synaptic function, short term synaptic plasticity that has a role in information processing can be affected in AD that was investigated in this study. Field excitatory post synaptic potential (fEPSP) from Stratum radiatum of CA1 neurons were recorded following Schaffer collateral stimulation in a rat model of Alzheimer’s disease (AD). 1 µl of Aβ 1-42 (5µg/µl) and 1 µl of ibotenic acid (5µg/µl) were injected in dorsal hippocampus of male rats for AD induction. For examining the short-term synaptic plasticity, paired pulse stimulations with inter pulse interval (IPI) of 20, 80, and 200 ms were applied and paired pulse index (PPI) was calculated. Results showed that although AD induction decreased basal synaptic responses especially at high stimulus intensity, this change was not significant (ANOVA; P>0.05). Also there were no significant changes in PPI of AD rats at different IPIs including 20 ms (%40.4±4.68, n=5), 80 ms (%129.8±4.1, n=5), and 200 ms (%129±6.8, n=5) in comparison with control ones (%75.2±5.08, %138±7.56, %108.4±2.09 respectively, n=5, P>0.05, unpaired t-test). Such results indicate that hippocampal Aβ treatment does not lead to impairment of basal synaptic response and short term synaptic plasticity.