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

 Introduction: 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. Materials and Methods: 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: 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). Conclusion: Such results indicate that hippocampal Aβ treatment does not lead to impairment of basal synaptic response and short term synaptic plasticity