The reemergence of long-term potentiation in aged Alzheimer's disease mouse model

Seonghoo Huh, Soo-Ji Baek, Kyung-Hwa Lee, Daniel J Whitcomb, Jihoon Jo, Seong Min Choi, Dong Hyun Kim, Man-Seok Park, Kun Ho Lee, Byeong C Kim

Research output: Contribution to journalArticle (Academic Journal)peer-review

30 Citations (Scopus)
369 Downloads (Pure)


Mouse models of Alzheimer's disease (AD) have been developed to study the pathophysiology of amyloid β protein (Aβ) toxicity, which is thought to cause severe clinical symptoms such as memory impairment in AD patients. However, inconsistencies exist between studies using these animal models, specifically in terms of the effects on synaptic plasticity, a major cellular model of learning and memory. Whereas some studies find impairments in plasticity in these models, others do not. We show that long-term potentiation (LTP), in the CA1 region of hippocampal slices from this mouse, is impared at Tg2576 adult 6-7 months old. However, LTP is inducible again in slices taken from Tg2576 aged 14-19 months old. In the aged Tg2576, we found that the percentage of parvalbumin (PV)-expressing interneurons in hippocampal CA1-3 region is significantly decreased, and LTP inhibition or reversal mediated by NRG1/ErbB signaling, which requires ErbB4 receptors in PV interneurons, is impaired. Inhibition of ErbB receptor kinase in adult Tg2576 restores LTP but impairs depotentiation as shown in aged Tg2576. Our study suggests that hippocampal LTP reemerges in aged Tg2576. However, this reemerged LTP is an insuppressible form due to impaired NRG1/ErbB signaling, possibly through the loss of PV interneurons.

Original languageEnglish
Article number29152
Number of pages10
JournalScientific Reports
Publication statusPublished - 5 Jul 2016


  • Inhibition–excitation balance
  • Long-term potentiation


Dive into the research topics of 'The reemergence of long-term potentiation in aged Alzheimer's disease mouse model'. Together they form a unique fingerprint.

Cite this