Non-fibrillar beta-amyloid abates spike-timing-dependent synaptic potentiation at excitatory synapses in layer 2/3 of the neocortex by targeting postsynaptic AMPA receptors

I. Shemer, C. Holmgren, R. Min, L. Fülöp, M. Zilberter, K.M. Sousa, T. Farkas, W. Härtig, B. Penke, N. Burnashev, H. Tanila, Z. Zilberter, T. Harkany, Yuri Zilberter

Research output: Contribution to journalArticleAcademicpeer-review

75 Citations (Scopus)


Cognitive decline in Alzheimer's disease (AD) stems from the progressive dysfunction of synaptic connections within cortical neuronal microcircuits. Recently, soluble amyloid β protein oligomers (Aβ
Original languageEnglish
Pages (from-to)2035-2047
Number of pages13
JournalEuropean Journal of Neuroscience
Issue number8
Publication statusPublished - Apr 2006


  • Action Potentials/drug effects
  • Age Factors
  • Alzheimer Disease
  • Amyloid beta-Peptides/chemistry
  • Amyloid beta-Protein Precursor/genetics
  • Animals
  • Animals, Newborn
  • Disease Models, Animal
  • Electric Stimulation/methods
  • Excitatory Amino Acid Agonists/pharmacology
  • Excitatory Postsynaptic Potentials/drug effects
  • Gene Expression
  • Immunohistochemistry/methods
  • Male
  • Mice
  • Mice, Transgenic
  • N-Methylaspartate/pharmacology
  • Neocortex/pathology
  • Patch-Clamp Techniques/methods
  • Pyramidal Cells/drug effects
  • RNA, Messenger/metabolism
  • Receptors, AMPA/classification
  • Reverse Transcriptase Polymerase Chain Reaction/methods
  • Synapses/drug effects
  • Time Factors
  • alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid/pharmacology

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