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Introduction: Synaptic plasticity is inappropriately affected in neurodegenerative diseases including Alzheimer’s disease (AD). In this study, we examined the effect of intrahippocampal amyloid-beta (Aβ1-40) on dentate gyrus long-term potentiation (LTP) and presynaptic short-term plasticity in a rat model of AD.
Methods: The experimental groups in this research study included a control with no treatment, sham-operated receiving the vehicle (normal saline), and Aβ[ma1] -lesioned. For modeling AD in Aβ[ma2]  group, aggregated A𝛽1-40 (10 mg/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 was taken as an index of long-term synaptic plasticity after application of high-frequency stimulation (HFS) to induce LTP in 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, the fEPSP slope and PS amplitude significantly decreased following the application of HFS in an amyloid beta-injected group. In addition, there was no significant difference between the control and sham-operated groups regarding the mentioned parameters.

Conclusion: The findings of this study clearly demonstrated that microinjection of amyloid beta1-40 into CA1 could impair LTP in dentate gyrus but could not modify short-term plasticity.

Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2018/05/26 | Accepted: 2018/07/24 | Published: 2018/03/15

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