Activation of p75NTR by proBDNF facilitates hippocampal long-term depression

By N. Woo, Henry K Teng, C. Siao, C. Chiaruttini, Petti T. Pang, T. Milner, B. Hempstead, B. Lu. Nature Neuroscience, 2005

814 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Developmental Neuroscience, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/a744a192afbcbe3f8f2c8dd24b383f66fe46c53d

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. B. Lu
2. Keri Martinowich
3. T. Rantamäki
4. L. Monteggia
5. Eero Castrén
6. Anita E. Autry
7. L. Reichardt
8. N. Woo

In Developmental Neuroscience

1. B. Lu
2. Eero Castrén
3. L. Monteggia
4. Anita E. Autry
5. T. Rantamäki
6. Keri Martinowich
7. N. Woo
8. Petti T. Pang

In Molecular Biology

1. B. Lu
2. L. Reichardt
3. Keri Martinowich
4. G. Lietzau
5. Janusz Morys
6. E. Czuba
7. Monika Waskow
8. A. Steliga

Citations in the corpus

• Brain-Derived Neurotrophic Factor and Neuropsychiatric Disorders (2012, background): “…is not an inactive precursor and has been shown to have effects in the central nervous system that are independent of mature BDNF. Recent data suggest that pro-BDNF and mature BDNF activate different intracellular signaling pathways (Woo et al., 2005; Matsumoto et al., 2008; Yang et al., 2009).”
• Long-term depression in the CNS (2010, background): “In addition, in young adult animals proBDNF (the precursor of brain-derived neurotrophic factor (BDNF)), acting via neurotrophin receptor P75 (p75 NTR ), increases GluN2B expression and so enables a GluN2B-sensitive form of NMDAR-LTD to occu”
• GDNF, NGF and BDNF as therapeutic options for neurodegeneration. (2013, background): “facilitates hippocampal LTD by increasing the NMDA receptor NR2B subunit (Woo et al., 2005).”
• BDNF: A Key Factor with Multipotent Impact on Brain Signaling and Synaptic Plasticity (2017, background): “Due to the reduction in the number of neurons and deterioration of synaptic function, these processes contribute to longterm depression (LTD), as revealed in hippocampal neurons (Park and Poo 2013; Woo et al. 2005; Yang et al. 2014).”
• Neurotrophin-regulated signalling pathways (2006, background): “…receptors has focused on signalling pathways initiated through phosphorylation of Y490 and Y785, analyses of mutant mice, homozygous for TrkB mutants in which F replaces Y at these sites, indicate that most of the additional docking sites have redundant roles in signalling (Minichiello et al.…”
• The role of BDNF and its receptors in depression and antidepressant drug action: Reactivation of developmental plasticity (2010, background): “The activation of p75NTR by pro-BDNF has been shown to induce neuronal atrophy and apoptosis, dendritic pruning and the induction of long-term depression (LTD) (Lee et al., 2001; Lu et al., 2005; Woo et al., 2005; Zagrebelsky et al., 2005).”
• The yin and yang of neurotrophin action (2005, background): “There is now evidence that proBDNF functions as an endogenous ligand for p75 NTR in the regulation of LT”
• Mouse and rat BDNF gene structure and expression revisited (2006, background): “Secreted proBDNF activates a heteromeric receptor complex of p75 and sortilin to initiate cell death (Teng et al., 2005) and binds to p75 in hippocampal neurons to enhance longterm depression (Woo et al., 2005).”
• New insights into BDNF function in depression and anxiety (2007, result): “Recent studies have demonstrated that proBDNF and mBDNF facilitate long-term depression (LTD) and long-term potentiation (LTP), respectively, implying opposing cellular function”
• A common polymorphism in the brain‐derived neurotrophic factor gene (BDNF) modulates human cortical plasticity and the response to rTMS (2008, background): “Brain-derived neurotrophic factor (BDNF) has a variety of roles in development and in the adult has been shown in animal models (Aicardi et al. 2004) to modulate NMDAR-dependent LTP (Figurov et al. 1996) and LTD (Woo et al. 2005a).”
• New insights in the biology of BDNF synthesis and release: implications in CNS function (2009, neutral): “Perfusion of uncleavable proBDNF significantly enhances LTD, an effect not observed in p75 NTR knock-out animals (Woo et al., 2005).”
• Post-synaptic BDNF-TrkB Signaling in Synapse Maturation, Plasticity and Disease (2010, neutral): “Long-term potentiation, also termed early LTP (E-LTP), and NMDAR-dependent long-term depression (LTD) of synaptic efficacy, elicited by a short period of synaptic stimulation, are partially mediated by local effects at the stimulated synapse, including the incorporation or removal of AMPARs and the ”