Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease
Brain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its re...
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| Format: | Article |
| Language: | en_US |
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Wiley-Blackwell Pubishers
2012
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| Online Access: | http://hdl.handle.net/1721.1/70067 https://orcid.org/0000-0003-2268-0863 |
| _version_ | 1811094704558702592 |
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| author | Yoshii, Akira Constantine-Paton, Martha |
| author2 | Massachusetts Institute of Technology. Department of Biology |
| author_facet | Massachusetts Institute of Technology. Department of Biology Yoshii, Akira Constantine-Paton, Martha |
| author_sort | Yoshii, Akira |
| collection | MIT |
| description | Brain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its receptor, full length TrkB. BDNF-TrkB signaling is involved in transcription, translation, and trafficking of proteins during various phases of synaptic development and has been implicated in several forms of synaptic plasticity. These functions are carried out by a combination of the three signaling cascades triggered when BDNF binds TrkB: The mitogen-activated protein kinase (MAPK), the phospholipase Cγ (PLC PLCγ), and the phosphatidylinositol 3-kinase (PI3K) pathways. MAPK and PI3K play crucial roles in both translation and/or trafficking of proteins induced by synaptic activity, whereas PLCγ regulates intracellular Ca2+ that can drive transcription via cyclic AMP and a protein kinase C. Conversely, the abnormal regulation of BDNF is implicated in various developmental and neurodegenerative diseases that perturb neural development and function. We will discuss the current state of understanding BDNF signaling in the context of synaptic development and plasticity with a focus on the postsynaptic cell and close with the evidence that basic mechanisms of BDNF function still need to be understood to effectively treat genetic disruptions of these pathways that cause devastating neurodevelopmental diseases. |
| first_indexed | 2024-09-23T16:03:44Z |
| format | Article |
| id | mit-1721.1/70067 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T16:03:44Z |
| publishDate | 2012 |
| publisher | Wiley-Blackwell Pubishers |
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| spelling | mit-1721.1/700672022-09-29T17:56:53Z Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease Yoshii, Akira Constantine-Paton, Martha Massachusetts Institute of Technology. Department of Biology Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences McGovern Institute for Brain Research at MIT Constantine-Paton, Martha Constantine-Paton, Martha Yoshii, Akira Brain-derived neurotrophic factor (BDNF) is a prototypic neurotrophin that regulates diverse developmental events from the selection of neural progenitors to the terminal dendritic differentiation and connectivity of neurons. We focus here on activity-dependent synaptic regulation by BDNF and its receptor, full length TrkB. BDNF-TrkB signaling is involved in transcription, translation, and trafficking of proteins during various phases of synaptic development and has been implicated in several forms of synaptic plasticity. These functions are carried out by a combination of the three signaling cascades triggered when BDNF binds TrkB: The mitogen-activated protein kinase (MAPK), the phospholipase Cγ (PLC PLCγ), and the phosphatidylinositol 3-kinase (PI3K) pathways. MAPK and PI3K play crucial roles in both translation and/or trafficking of proteins induced by synaptic activity, whereas PLCγ regulates intracellular Ca2+ that can drive transcription via cyclic AMP and a protein kinase C. Conversely, the abnormal regulation of BDNF is implicated in various developmental and neurodegenerative diseases that perturb neural development and function. We will discuss the current state of understanding BDNF signaling in the context of synaptic development and plasticity with a focus on the postsynaptic cell and close with the evidence that basic mechanisms of BDNF function still need to be understood to effectively treat genetic disruptions of these pathways that cause devastating neurodevelopmental diseases. United States. Dept. of Defense (contract grant number: TS080074) National Institutes of Health (U.S.) (Contract grant number: R01EY014074) National Institutes of Health (U.S.) (Contract grant number: R01EY006039) 2012-04-19T18:36:36Z 2012-04-19T18:36:36Z 2010-02 2009-10 Article http://purl.org/eprint/type/JournalArticle 1932-8451 1932-846X http://hdl.handle.net/1721.1/70067 Yoshii, Akira, and Martha Constantine-Paton. “Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease.” Developmental Neurobiology (2010): 304–322. https://orcid.org/0000-0003-2268-0863 en_US http://dx.doi.org/10.1002/dneu.20765 Developmental Neurobiology Creative Commons Attribution-Noncommercial-Share Alike 3.0 http://creativecommons.org/licenses/by-nc-sa/3.0/ application/pdf Wiley-Blackwell Pubishers PubMed Central |
| spellingShingle | Yoshii, Akira Constantine-Paton, Martha Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease |
| title | Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease |
| title_full | Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease |
| title_fullStr | Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease |
| title_full_unstemmed | Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease |
| title_short | Postsynaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity, and Disease |
| title_sort | postsynaptic bdnf trkb signaling in synapse maturation plasticity and disease |
| url | http://hdl.handle.net/1721.1/70067 https://orcid.org/0000-0003-2268-0863 |
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