Tyler WJ, Alonso M, Bramham CR, Pozzo-Miller LD. From acquisition to consolidation: on the role of brain-derived neurotrophic factor signaling in hippocampal-dependent learning. Learn Mem 9: 224-237

Departments of Neurobiology and Psychology, Civitan International Research Center, University of Alabama at Birmingham, Birmingham, Alabama 35294-0021, USA.
Learning &amp Memory (Impact Factor: 3.66). 09/2002; 9(5):224-37. DOI: 10.1101/lm.51202
Source: PubMed


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.

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Available from: Lucas Pozzo-Miller, Dec 17, 2013
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    • "Notably, TRPC3 channels have been described as mediators of BDNF-mediated dendritic remodeling in hippocampal CA1 pyramidal neurons [141]. BDNF plays a significant role in modulating synaptic plasticity (reviewed in [142]) by enhancing synaptic transmission at excitatory synapses and altering dendritic architecture [143]. The role of interactions between STIM1 proteins and TRPC channels is under vigorous investigation (reviewed in [73]). "
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