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Fluoxetine Inhibits Natural Decay of Long-Term Memory via Akt/GSK-3β Signaling

Research output: Contribution to journalArticle

  • Jee Hyun Yi
  • Jia Bao Zhang
  • Sang Yoon Ko
  • Huiyoung Kwon
  • Se Jin Jeon
  • Se Jin Park
  • Jiwook Jung
  • Byung C. Kim
  • Young Choon Lee
  • Dong Hyun Kim
  • Jong Hoon Ryu
Original languageEnglish
Pages (from-to)1-10
Number of pages10
JournalMolecular Neurobiology
DOIs
DateE-pub ahead of print - 9 Feb 2018

Abstract

Understanding the mechanisms underlying the natural decay of long-term memory can help us find means of extending the duration of long-term memory. However, the neurobiological processes involved in the decay of long-term memory are poorly understood. In the present study, we examined the effect of acute and chronic treatment of fluoxetine on natural decay of long-term memory and the possible mechanism. Late administration of fluoxetine prolonged the persistence of long-term memory in mice, as demonstrated by object location recognition and Barnes maze tests. Fluoxetine altered Akt/glycogen synthase kinase-3β (GSK-3β)/β-catenin signaling in the hippocampus. Late short- and long-term pharmacological inhibition of GSK-3β mimicked the effect of fluoxetine on memory persistence. Pharmacological inhibition of Akt blocked the effect of fluoxetine on memory persistence. Finally, late infusion of fluoxetine increased hippocampal long-term potentiation (LTP) and pharmacological inhibition of GSK-3β blocked the natural decline in LTP. These results demonstrate that GSK-3β might be a key molecule in memory decay process, and fluoxetine extends the period of long-term memory maintenance via Akt/GSK-3β signaling.

    Research areas

  • Fluoxetine, GSK-3β, LTP maintenance, Memory decay

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