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Aß Facilitates LTD at Schaffer Collateral Synapses Preferentially in the Left Hippocampus
Kenneth J O'Riordan1, Neng-Wei Hu2, Michael J Rowan1
1Department of Pharmacology and Therapeutics and Institute of Neuroscience, Watts Building, Trinity College, Dublin 2, Ireland.
Cell Reports
|February 22, 2018
Summary
Soluble amyloid-beta oligomers promote long-term depression (LTD) in Alzheimer's disease. This study shows amyloid-beta enhances LTD in the left hippocampus, potentially explaining aberrant brain lateralization in Alzheimer's disease.
Area of Science:
- Neuroscience
- Synaptic Plasticity
- Alzheimer's Disease Research
Background:
- Synaptic dysfunction in Alzheimer's disease (AD) is linked to amyloid-beta (Aß) oligomers promoting long-term depression (LTD).
- Previous LTD induction methods lacked physiological specificity.
Purpose of the Study:
- To investigate LTD mechanisms using optogenetics for precise pathway activation in vivo.
- To explore the role of Aß in circuit-selective synaptic plasticity and hippocampal asymmetry.
Main Methods:
- Utilized optogenetics for spatially defined pathway activation in the rat hippocampus.
- Examined LTD induction requirements, including NMDA receptor subunits and modulatory receptors.
- Assessed the impact of Aß on LTD in a lateralized manner.
Main Results:
- Sparse synaptic LTD requires NMDA receptor ion channel function and the GluN2B subunit.
- Unlike electrically induced LTD, optogenetically induced LTD is not facilitated by muscarinic acetylcholine or mGluR5 activation.
- Amyloid-beta preferentially enhances LTD in the left hippocampus via mGluR5, creating asymmetry.
Conclusions:
- Optogenetics enables studying physiologically relevant LTD patterns.
- Amyloid-beta induces circuit-selective disruption of synaptic plasticity.
- Aß-mediated hippocampal asymmetry offers insights into aberrant brain lateralization in Alzheimer's disease.
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