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. 2020 Jul-Aug;11(4):517-524.
doi: 10.32598/bcn.9.10.190. Epub 2020 Jul 1.

Differential Effect of Amyloid Beta1-40 on Short-term and Long-term Plasticity in Dentate Gyrus of a Rat Model of Alzheimer Disease

Javad Fahanik-Babaei  1 , Tourandokht Baluchnejadmojarad  1   2 , Mehrdad Roghani  3
Affiliations

Differential Effect of Amyloid Beta1-40 on Short-term and Long-term Plasticity in Dentate Gyrus of a Rat Model of Alzheimer Disease

Javad Fahanik-Babaei et al. Basic Clin Neurosci. 2020 Jul-Aug.

Abstract

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 Long-term Potentiation (LTP) and presynaptic short-term plasticity in a rat model of AD.

Methods: The experimental groups in this research included the control with no treatment, sham-operated 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 long-term 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.

Keywords: Alzheimer disease; Amyloid beta; Synaptic plasticity.

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Conflict of interest statement

Conflict of interest The authors declared no conflict of interest.

Figures

Figure 1.
Figure 1.
The input-output curves shown as field Excitatory Post-Synaptic Potential (fEPSP) slope and Population Spike (PS) amplitude in the dentate gyrus Each point represents data obtained from 6 rats. Specimen recordings showed changes in baseline and LTP recordings 60 min after high-frequency stimulation HFS. Each recording is the average of 10 consecutive recordings at 100 s with an interval of 10 s. There was no statistically significant difference amongst the groups.
Figure 2.
Figure 2.
The effect of Amyloid-Beta (Aβ1-40) on paired-pulse responses in the hippocampal dentate gyrus At the intervals of 10, 20, 30, and 50, as shown by field Excitatory Post-Synaptic Potential (fEPSP) slope ratio (second response/ first response ratio) and Population Spike (PS) amplitude ratio (second response/first response ratio) (n=6 per group) and traces recorded at dentate gyrus at an inter-stimulus interval of 50 ms. There was no statistically significant difference amongst the groups. Recording of the average of 10 consecutive PSs evoked by the paired stimuli in 100 s.
Figure 3.
Figure 3.
The effect of amyloid-beta (Aβ1-40) on long-term potentiation (LTP) in the hippocampal dentate gyrus using High-Frequency Stimulation (HFS) as shown by field Excitatory Post-Synaptic Potential (fEPSP) slope and Population Spike (PS) amplitude and representative traces of evoked responses in the dentate gyrus of the rat hippocampus following stimulation of the medial perforant path; (n=6 per group); *P<0.05; and **P<0.01 versus the control group.
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