Brain-derived neurotrophic factor/TrkB signaling in memory processes

Kiyofumi Yamada, Toshitaka Nabeshima

Research output: Contribution to journalReview article

352 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)267-270
Number of pages4
JournalJournal Pharmacological Sciences
Volume91
Issue number4
DOIs
Publication statusPublished - 01-04-2003
Externally publishedYes

Fingerprint

Brain-Derived Neurotrophic Factor
trkB Receptor
Learning
Hippocampus
Neuronal Plasticity
src-Family Kinases
Long-Term Potentiation
Phosphatidylinositols
Mitogen-Activated Protein Kinases
N-Methyl-D-Aspartate Receptors
Fear
Phosphotransferases
Messenger RNA

All Science Journal Classification (ASJC) codes

  • Molecular Medicine
  • Pharmacology

Cite this

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abstract = "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.",
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Brain-derived neurotrophic factor/TrkB signaling in memory processes. / Yamada, Kiyofumi; Nabeshima, Toshitaka.

In: Journal Pharmacological Sciences, Vol. 91, No. 4, 01.04.2003, p. 267-270.

Research output: Contribution to journalReview article

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