Amyloid-β (25–35) induces the morphological alteration of dendritic spines and decreases NR2B and PSD-95 expression in the hippocampus

• Published in: Neuroscience letters 2023-01, Vol.795, p.137030-137030, Article 137030
• Main Authors: Ramírez-Hernández, Eleazar, Sánchez-Maldonado, Claudia, Patricio-Martínez, Aleidy, Limón, Ilhiucamina Daniel
• Format: Article
• Language: English
• Subjects: Alzheimer Disease - metabolism; Amyloid beta-Peptides - metabolism; Animals; Aβ25–35; Dendritic spines; Dendritic Spines - metabolism; Disks Large Homolog 4 Protein - metabolism; Hippocampus; Hippocampus - metabolism; Learning and memory; Maze Learning; Memory Disorders - metabolism; NR2B subunit of NMDA receptor; Peptide Fragments - metabolism; Peptide Fragments - pharmacology; PSD-95; Rats; Spatial Memory
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/j.neulet.2022.137030

[Display omitted] •The Aβ25–35 induces impairment in the retrieval of memory associated with changes to the morphology of dendritic spines.•The Aβ25–35 decreases the number of dendritic spines and the changes in NR2B and PSD-95 expression in the hippocampus.•The Aβ25–35 perturbs synaptic plasticity, in the formation of new synapses, promoting the progression of memory impairment. Research on the memory impairment caused by the Amyloid-β 25–35 (Aβ25–35) peptide in animal models has provided an understanding of the causes that occurs in Alzheimer’s disease. However, it is uncertain whether this cognitive impairment occurs due to disruption of information encoding and consolidation or impaired retrieval of stored memory. The aim of this study was to determine the effect of the Aβ25–35 peptide on the morphology of dendritic spines and the changes in the expression of NR2B and PSD-95 in the hippocampus associated with learning and memory deficit. Vehicle or Aβ25–35 peptide (0.1 µg/µL) was bilaterally administered into the CA1 subfield of the rat hippocampus, then tested for spatial learning and memory in the Morris Water Maze. On Day 39, the morphological changes in the CA1 of the hippocampus and dentate gyrus were examined via Golgi-Cox stain. It was observed that the Aβ25–35 peptide administered in the CA1 region of the rat hippocampus induced changes to the morphology of dendritic spines and the expression of the NR2B subunit of the NMDA receptor co-localized with both the spatial memory and PSD-95 protein in the hippocampus of learning rats. We conclude that, in soluble form, the Aβ25–35 peptide perturbs synaptic plasticity, specifically in the formation of new synapses, thus promoting the progression of memory impairment.