Brain-derived neurotrophic factor/TrkB signaling in memory processes

Kiyofumi Yamada, Toshitaka Nabeshima

研究成果: Review article

360 引用 (Scopus)

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Activity-dependent changes in synaptic strength are considered mechanisms underlying learning and memory. Brain-derived neurotrophic factor (BDNF) plays an important role in activity-dependent synaptic plasticity such as long-term potentiation. Recent experimental evidence supports the role of BDNF in memory processes: Memory acquisition and consolidation are associated with an increase in BDNF mRNA expression and the activation of its receptor TrkB. Genetic as well as pharmacologic deprivation of BDNF or TrkB impairs learning and memory. In a positively motivated radial arm maze test, activation of the TrkB/phosphatidyl-inositol-3 kinase (PI3-K) signaling pathway in the hippocampus is associated with consolidation of spatial memory through an activation of translational processes. In a negatively motivated passive avoidance test, mitogen-activated protein kinase (MAPK) is activated during acquisition of fear memory. Furthermore, recent findings suggest the importance of interaction between BDNF/TrkB signaling and NMDA receptors for spatial memory. A Src-family tyrosine kinase, Fyn plays a role in this interaction by linking TrkB with NR2B. These findings suggest that BDNF/TrkB signaling in the hippocampus plays a crucial role in learning and memory.

元の言語English
ページ(範囲)267-270
ページ数4
ジャーナルJournal Pharmacological Sciences
91
発行部数4
DOI
出版物ステータスPublished - 01-04-2003
外部発表Yes

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All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

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