Role for brain-derived neurotrophic factor in learning and memory

Yamada, Kiyofumi; Mizuno, Makoto; Nabeshima, Toshitaka

doi:10.1016/s0024-3205(01)01461-8

Cited by 376 publications

(215 citation statements)

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“…In the context of the physiological role of BDNF, this apparent 'loss of function' is expected; increased BDNF is associated with activity, 40,41 cell survival, [42][43][44] learning and memory, 45 synaptic plasticity, 46,47 increased synthesis of mRNA and other processes that can be looked upon as 'positive' cellular events. Loss of BDNF would therefore be expected to decrease the expression of genes that mediate these effects.…”

Section: Discussionmentioning

confidence: 99%

Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood

et al. 2006

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Section: Discussionmentioning

confidence: 99%

Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood

et al. 2006

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“…The binding of Brain-derived neurotrophic factor (BDNF) [1][2][3][4] to its receptor tyrosine kinase B (TrkB) leads to autophosphorylation of tyrosine residues in the intracellular domain of the receptor and subsequent activation of cytoplasmic signaling pathways. Tyrosine phosphorylated TrkB serves as a scaffold for the recruitment of adaptor proteins and enzymes, including mitogen-associated protein kinase (MAPK), phospholipase C-g (PLC-g) and PI3-K that further transduce the BDNF signal.…”

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confidence: 99%

Phosphatidylinositol 3-kinase: a molecule mediating BDNF-dependent spatial memory formation

et al. 2003

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Brain-derived neurotrophic factor (BDNF) plays a critical role in synaptic plasticity such as long-term potentiation (LTP), a form of synaptic correlate of learning and memory. BDNF is also implicated in learning and memory. We have demonstrated that radial arm maze training in rats for spatial learning and memory results in a significant increase in the BDNF mRNA expression in the hippocampus. Moreover, antisense BDNF oligonucleotide treatment impaired not only acquisition, but also maintenance and/or recall of spatial memory in the maze. Although these results suggest a role of BDNF for spatial memory processes, the signal transduction mechanisms that mediate the actions of BDNF remain unknown. Here we show that phosphorylation of BDNF receptor tyrosine kinase B (TrkB), phosphatidylinositol 3-kinase (PI3-K) and Akt, a target of PI3-K, in the hippocampus increased in parallel with spatial memory formation. Moreover, an activation of translational processes was suggested in the hippocampus after the maze training. When spatial learning was inhibited by antisense BDNF oligodeoxynucleotide, the activation was diminished. Chronic treatment with PI3-K inhibitor wortmannin impaired spatial learning. Our findings suggested that activation of TrkB/PI3-K and protein synthesis signaling pathway by BDNF in the hippocampus is important for spatial memory.

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“…BDNF is widely expressed in the hippocampus and cerebral cortex (Hofer, Pagliusi, Hohn, Leibrock, & Barde, 1990; Huang & Reichardt, 2001) and enhances hippocampal long-term potentiation (Figurov, Pozzo-Miller, Olafsson, Wang, & Lu, 1996) associated with both memory and learning efficiency (Hariri et al, 2003; Yamada, Mizuno, & Nabeshima, 2002). The gene encoding BDNF contains a functional single-nucleotide polymorphism (SNP) resulting in a valine (val) to methionine (met) substitution at amino acid 66 ( Val66Met , rs6265) in the 5ʹ pro-BDNF domain (Egan et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

Martin

Hemmings

Kidd

et al. 2018

European Journal of Psychotraumatology

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Background: Anxiety disorders in youth are attributable to multiple causal mechanisms, comprising biological vulnerabilities, such as genetics and temperament, and unfavourable environmental influences, such as childhood maltreatment (CM).Objective: A gene-environment (G x E) interaction study was conducted to determine the interactive effect of the BDNF Val66Met polymorphism and CM to increase susceptibility to anxiety sensitivity (AS) in a sample of mixed race adolescents.Method: Participants (n = 308, mean age = 15.8 years) who were all secondary school students and who completed measures for AS and CM were genotyped for the BDNF Val66Met polymorphism. Hierarchical multiple regression analysis was conducted to assess G x E influences on AS. Age and gender were included in the models as covariates as age was significantly associated with AS total score (p < .05), and females had significantly higher AS scores than males (p < .05).Results: A main effect of CM on AS was evident (p < .05), however, no main effect of BDNF genotype on AS was observed (p > .05). A non-significant G x E effect on AS was revealed (p < .05).Conclusions: Our results suggest that CM does not have a moderating role in the relationship between the BDNF Val66Met genotype and the increased risk of anxiety-related phenotypes, such as AS. Given the exploratory nature of this study, findings require replication in larger samples and adjustment for population stratification to further explore the role of BDNF Val66Met and CM on AS in mixed race adolescents.

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Role for brain-derived neurotrophic factor in learning and memory

Cited by 376 publications

References 0 publications

Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood

Specificity and timing of neocortical transcriptome changes in response to BDNF gene ablation during embryogenesis or adulthood

Phosphatidylinositol 3-kinase: a molecule mediating BDNF-dependent spatial memory formation

No gene-by-environment interaction of BDNF Val66Met polymorphism and childhood maltreatment on anxiety sensitivity in a mixed race adolescent sample

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