differential effect of amyloid beta1-40 on short-term and long-term plasticity in dentate gyrus of a rat model of alzheimer disease

Introduction: synaptic plasticity is inappropriately affected by neurodegenerative diseases, including alzheimer disease (ad). in this study, we examined the effect of intrahippocampal amyloid-beta (aβ1-40) on dentate gyrus longterm potentiation (ltp) and presynaptic shortterm plasticity in a rat model of ad. methods: the experimental groups in this research included the control with no treatment, shamoperated receiving the vehicle (normal saline), and aβ-lesioned groups. for modeling ad, aggregated aβ1-40 (10 µg/2 µl on each side) was injected into the hippocampal ca1. three weeks later, population spike (ps) amplitude and slope ratios were determined at different inter-pulse intervals (ipi) of 10, 20, 30, and 50 ms as a valid indicator of the short-term presynaptic facilitation and/or depression. in addition, ps amplitude and slope were taken as an index of longterm synaptic plasticity after application of high-frequency stimulation (hfs) to induce ltp in the medial perforant-dentate gyrus pathway. results: no significant differences were noted amongst the experimental groups regarding fepsp slope and paired-pulse indices as indicators of short-term plasticity. in contrast, fepsp slope and ps amplitude significantly decreased following the application of hfs in aβ-injected group. in addition, there was no significant difference between the control and sham-operated groups regarding the mentioned parameters. conclusion: findings of this study clearly demonstrated that microinjection of aβ1-40 into the ca1 could impair ltp in dentate gyrus but could not modify short-term plasticity.