Abstract
The effects of Alzheimer's disease-related beta-amyloid (Aβ) peptides on the N-methyl-D-aspartate (NMDA)-evoked cell firing rate were studied in hippocampal CA1 neurons of the rat. Extracellular single-unit recordings were combined with iontophoretic applications that allowed quantitative analyses of the interactions between Aβ peptides and NMDA receptor-mediated events in vivo. The NMDA responses were significantly increased both by the full length Aβ1-42 and by its model fragment Aβ25-35. Enhancements of the NMDA responses by the Aβ peptides lasted about 15 min and were irreversible. The effects of Aβ25-35 were prevented by the pentapeptide Lys-Leu-Val-Gly-Phe- amide (KLVGF) and were not evoked when its reversed sequence (Aβ35-25) was applied.
Original language | English |
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Pages (from-to) | 1649-1652 |
Number of pages | 4 |
Journal | Neuroreport |
Volume | 15 |
Issue number | 10 |
DOIs | |
Publication status | Published - 19 Jul 2004 |
Externally published | Yes |
Keywords
- Alzheimer's disease
- Amyloid β-peptide
- Amyloid fragment
- Microiontophoresis
- NMDA
- Rat
- Single-unit recording
ASJC Scopus subject areas
- General Neuroscience