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Open AccessArticle

Impairments of Synaptic Plasticity Induction Threshold and Network Oscillatory Activity in the Hippocampus Underlie Memory Deficits in a Non-Transgenic Mouse Model of Amyloidosis

1
Neurophysiology and Behavioral Lab, Centro Regional de Investigaciones Biomédicas, School of Medicine of Ciudad Real, University of Castilla-La Mancha, 13071 Ciudad Real, Spain
2
Division of Neurosciences, Pablo de Olavide University, 41013 Seville, Spain
*
Authors to whom correspondence should be addressed.
Current Address: Geriatric Department, Instituto Investigación Sanitaria Gregorio Marañón, Consorcio de Investigación Biomédica en Red: Fragilidad y Envejecimiento Saludable, CIBERFES, 28007 Madrid, Spain.
These authors contributed equally to this work.
Biology 2020, 9(7), 175; https://doi.org/10.3390/biology9070175
Received: 9 June 2020 / Revised: 7 July 2020 / Accepted: 17 July 2020 / Published: 20 July 2020
(This article belongs to the Special Issue Brain Damage and Repair: From Molecular Effects to CNS Disorders)
In early Alzheimer disease (AD) models synaptic failures and upstreaming aberrant patterns of network synchronous activity result in hippocampal-dependent memory deficits. In such initial stage, soluble forms of Amyloid-β (Aβ) peptides have been shown to play a causal role. Among different Aβ species, Aβ25–35 has been identified as the biologically active fragment, as induces major neuropathological signs related to early AD stages. Consequently, it has been extensively used to acutely explore the pathophysiological events related with neuronal dysfunction induced by soluble Aβ forms. However, the synaptic mechanisms underlying its toxic effects on hippocampal-dependent memory remain unresolved. Here, in an in vivo model of amyloidosis generated by intracerebroventricular injections of Aβ25–35 we studied the synaptic dysfunction mechanisms underlying hippocampal cognitive deficits. At the synaptic level, long-term potentiation (LTP) of synaptic excitation and inhibition was induced in CA1 region by high frequency simulation (HFS) applied to Schaffer collaterals. Aβ25–35 was found to alter metaplastic mechanisms of plasticity, facilitating long-term depression (LTD) of both types of LTP. In addition, aberrant synchronization of hippocampal network activity was found while at the behavioral level, deficits in hippocampal-dependent habituation and recognition memories emerged. Together, our results provide a substrate for synaptic disruption mechanism underlying hippocampal cognitive deficits present in Aβ25–35 amyloidosis model. View Full-Text
Keywords: Alzheimer model; amyloid-β; hippocampus; in vivo; synaptic plasticity; metaplasticity; oscillatory activity; electrophysiology; behavior; novel object recognition; habituation; LTP; LTD Alzheimer model; amyloid-β; hippocampus; in vivo; synaptic plasticity; metaplasticity; oscillatory activity; electrophysiology; behavior; novel object recognition; habituation; LTP; LTD
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MDPI and ACS Style

Mayordomo-Cava, J.; Iborra-Lázaro, G.; Djebari, S.; Temprano-Carazo, S.; Sánchez-Rodríguez, I.; Jeremic, D.; Gruart, A.; Delgado-García, J.M.; Jiménez-Díaz, L.; Navarro-López, J.D. Impairments of Synaptic Plasticity Induction Threshold and Network Oscillatory Activity in the Hippocampus Underlie Memory Deficits in a Non-Transgenic Mouse Model of Amyloidosis. Biology 2020, 9, 175. https://doi.org/10.3390/biology9070175

AMA Style

Mayordomo-Cava J, Iborra-Lázaro G, Djebari S, Temprano-Carazo S, Sánchez-Rodríguez I, Jeremic D, Gruart A, Delgado-García JM, Jiménez-Díaz L, Navarro-López JD. Impairments of Synaptic Plasticity Induction Threshold and Network Oscillatory Activity in the Hippocampus Underlie Memory Deficits in a Non-Transgenic Mouse Model of Amyloidosis. Biology. 2020; 9(7):175. https://doi.org/10.3390/biology9070175

Chicago/Turabian Style

Mayordomo-Cava, Jennifer; Iborra-Lázaro, Guillermo; Djebari, Souhail; Temprano-Carazo, Sara; Sánchez-Rodríguez, Irene; Jeremic, Danko; Gruart, Agnès; Delgado-García, José M.; Jiménez-Díaz, Lydia; Navarro-López, Juan D. 2020. "Impairments of Synaptic Plasticity Induction Threshold and Network Oscillatory Activity in the Hippocampus Underlie Memory Deficits in a Non-Transgenic Mouse Model of Amyloidosis" Biology 9, no. 7: 175. https://doi.org/10.3390/biology9070175

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