From acquisition to consolidation

On the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning

William Tyler, Mariana Alonso, Clive R. Bramham, Lucas D. Pozzo-Miller

Research output: Contribution to journalArticle

480 Citations (Scopus)

Abstract

One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short- and long-term periods of enhanced synaptic physiology in both pre- and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.

Original languageEnglish (US)
Pages (from-to)224-237
Number of pages14
JournalLearning and Memory
Volume9
Issue number5
DOIs
StatePublished - Sep 2002
Externally publishedYes

Fingerprint

Brain-Derived Neurotrophic Factor
Learning
Neuronal Plasticity
Synaptic Transmission
Neurosciences
Synapses
Phosphotransferases
Central Nervous System

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

From acquisition to consolidation : On the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning. / Tyler, William; Alonso, Mariana; Bramham, Clive R.; Pozzo-Miller, Lucas D.

In: Learning and Memory, Vol. 9, No. 5, 09.2002, p. 224-237.

Research output: Contribution to journalArticle

Tyler, William ; Alonso, Mariana ; Bramham, Clive R. ; Pozzo-Miller, Lucas D. / From acquisition to consolidation : On the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning. In: Learning and Memory. 2002 ; Vol. 9, No. 5. pp. 224-237.
@article{0b0a989a49174d349c466dbbdb4542eb,
title = "From acquisition to consolidation: On the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning",
abstract = "One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short- and long-term periods of enhanced synaptic physiology in both pre- and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.",
author = "William Tyler and Mariana Alonso and Bramham, {Clive R.} and Pozzo-Miller, {Lucas D.}",
year = "2002",
month = "9",
doi = "10.1101/lm.51202",
language = "English (US)",
volume = "9",
pages = "224--237",
journal = "Learning & memory (Cold Spring Harbor, N.Y.)",
issn = "1072-0502",
publisher = "Cold Spring Harbor Laboratory Press",
number = "5",

}

TY - JOUR

T1 - From acquisition to consolidation

T2 - On the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning

AU - Tyler, William

AU - Alonso, Mariana

AU - Bramham, Clive R.

AU - Pozzo-Miller, Lucas D.

PY - 2002/9

Y1 - 2002/9

N2 - One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short- and long-term periods of enhanced synaptic physiology in both pre- and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.

AB - One of the most rigorously investigated problems in modern neuroscience is to decipher the mechanisms by which experience-induced changes in the central nervous system are translated into behavioral acquisition, consolidation, retention, and subsequent recall of information. Brain-derived neurotrophic factor (BDNF) has recently emerged as one of the most potent molecular mediators of not only central synaptic plasticity, but also behavioral interactions between an organism and its environment. Recent experimental evidence indicates that BDNF modulates synaptic transmission and plasticity by acting across different spatial and temporal domains. BDNF signaling evokes both short- and long-term periods of enhanced synaptic physiology in both pre- and postsynaptic compartments of central synapses. Specifically, BDNF/TrkB signaling converges on the MAP kinase pathway to enhance excitatory synaptic transmission in vivo, as well as hippocampal-dependent learning in behaving animals. Emerging concepts of the intracellular signaling cascades involved in synaptic plasticity induced through environmental interactions resulting in behavioral learning further support the contention that BDNF/TrkB signaling plays a fundamental role in mediating enduring changes in central synaptic structure and function. Here we review recent literature showing the involvement of BDNF/TrkB signaling in hippocampal-dependent learning paradigms, as well as in the types of cellular plasticity proposed to underlie learning and memory.

UR - http://www.scopus.com/inward/record.url?scp=0036742611&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0036742611&partnerID=8YFLogxK

U2 - 10.1101/lm.51202

DO - 10.1101/lm.51202

M3 - Article

VL - 9

SP - 224

EP - 237

JO - Learning & memory (Cold Spring Harbor, N.Y.)

JF - Learning & memory (Cold Spring Harbor, N.Y.)

SN - 1072-0502

IS - 5

ER -