NMDA-receptor activation but not ion flux is required for amyloid-beta induced synaptic depression.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 23750255.
- Also identified by DOI 10.1371/journal.pone.0065350 and PMC identifier 3672194.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Alzheimer disease is characterized by a gradual decrease of synaptic function and, ultimately, by neuronal loss. There is considerable evidence supporting the involvement of oligomeric amyloid-beta (Aβ) in the etiology of Alzheimer's disease. Historically, AD research has mainly focused on the long-term changes caused by Aβ rather than analyzing its immediate effects. Here we show that acute perfusion of hippocampal slice cultures with oligomeric Aβ depresses synaptic transmission within 20 minutes. This depression is dependent on synaptic stimulation and the activation of NMDA-receptors, but not on NMDA-receptor mediated ion flux. It, therefore, appears that Aβ dependent synaptic depression is mediated through a use-dependent metabotropic-like mechanism of the NMDA-receptor, but does not involve NMDA-receptor mediated synaptic transmission, i.e. it is independent of calcium flux through the NMDA-receptor.
Medical subject headings
- Amyloid beta-Peptides
- Peptide Fragments
- Receptors, N-Methyl-D-Aspartate
- Synapses
- Synaptic Transmission