Age‐related synaptic dysfunction in Tg2576 mice starts as a failure in early long‐term potentiation which develops into a full abolishment of late long‐term potentiation

• DOI: 10.1002/jnr.23701
• Publication Date: 2015-12-02T13:42:50Z
• Authors: Diego Fernández‐F...; Cornelia Dorner‐C...; Katja S. Kroker; Holger Rosenbrock
• Keywords: Neural facilitation

Tg2576 mice are widely used to study amyloid-dependent synaptic dysfunction related Alzheimer's disease. However, conflicting data have been reported for these with regard basal transmission as well the in vitro correlate of memory, long-term potentiation (LTP). Some studies show clear impairments, whereas others report no deficiency. The present uses hippocampal slices from 3-, 10-, and 15-month-old wild-type (WT) evaluate function each group, including experiments investigate transmission, short- plasticity by inducing paired-pulse facilitation, both early late LTP. We that remains intact at 3 months age. LTP decline progressively during aging mice. This deterioration starts affecting LTP, ultimately leading abolishment forms animals. In comparison, WT littermates display normal parameters aging. Additional pharmacological investigation into involvement NMDA receptors L-type voltage-gated calcium channels suggests a distinct mechanism induction among age groups, demonstrating differentially affected