ArticleNeural plasticity2012
Divergent roles of p75NTR and Trk receptors in BDNF's effects on dendritic spine density and morphology.
Article in Neural plasticity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 57 citations in OpenAlex.
- Taming the "death receptor": translating the first-in-class p75Journal of translational medicine · 2026Review
- Neural Influences on Tumor Progression Within the Central Nervous System.CNS neuroscience & therapeutics · 2024Review
- A small-molecule TrkB ligand improves dendritic spine phenotypes and atypical behaviors in female Rett syndrome mice.Disease models & mechanisms · 2024Article
- Are TrkB receptor agonists the right tool to fulfill the promises for a therapeutic value of the brain-derived neurotrophic factor?Neural regeneration research · 2024Review
- Article
- Neuron-derived extracellular vesicles contain synaptic proteins, promote spine formation, activate TrkB-mediated signalling and preserve neuronal complexity.Journal of extracellular vesicles · 2023Article
- Mitochondria as central hubs in synaptic modulation.Cellular and molecular life sciences : CMLS · 2023Review
- Neurotrophic Factors and Dendritic Spines.Advances in neurobiology · 2023Article
- Interactions Among Brain-Derived Neurotrophic Factor and Neuroimmune Pathways Are Key Components of the Major Psychiatric Disorders.Molecular neurobiology · 2022Review
- Chronic partial TrkB activation reduces seizures and mortality in a mouse model of Dravet syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Actions of the TrkB Agonist Antibody ZEB85 in Regulating the Architecture and Synaptic Plasticity in Hippocampal Neurons.Frontiers in molecular neuroscience · 2022Article
- Neuronal apoptosis induced by morphine withdrawal is mediated by the p75 neurotrophin receptor.Journal of neurochemistry · 2021Article
- Partial Activation of TrkB Receptors Corrects Interneuronal Calcium Channel Dysfunction and Reduces Epileptogenic Activity in Neocortex following Injury.Cerebral cortex (New York, N.Y. : 1991) · 2020Article
- Reversal of Cognitive Impairment in gp120 Transgenic Mice by the Removal of the p75 Neurotrophin Receptor.Frontiers in cellular neuroscience · 2019Article
- Distinct effects on the dendritic arbor occur by microbead versus bath administration of brain-derived neurotrophic factor.Cellular and molecular life sciences : CMLS · 2017Article
- BDNF-TrkB controls cocaine-induced dendritic spines in rodent nucleus accumbens dissociated from increases in addictive behaviors.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- The neurotrophin receptor p75 mediates gp120-induced loss of synaptic spines in aging mice.Neurobiology of aging · 2016Article
- The Neurotrophic Factor Receptor p75 in the Rat Dorsolateral Striatum Drives Excessive Alcohol Drinking.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- The requirement of BDNF for hippocampal synaptic plasticity is experience-dependent.Hippocampus · 2016Article
- Expression of gp120 in mice evokes anxiety behavior: Co-occurrence with increased dendritic spines and brain-derived neurotrophic factor in the amygdala.Brain, behavior, and immunity · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Activation of TrkB receptors by brain-derived neurotrophic factor (BDNF) followed by MAPK/ERK signaling increases dendritic spine density and the proportion of mature spines in hippocampal CA1 pyramidal neurons. Considering the opposing actions of p75(NTR) and Trk receptors in several BDNF actions on CNS neurons, we tested whether these receptors also have divergent actions on dendritic spine density and morphology. A function-blocking anti-p75(NTR) antibody (REX) did not affect spine density by itself but it prevented BDNF's effect on spine density. Intriguingly, REX by itself increased the proportion of immature spines and prevented BDNF's effect on spine morphology. In contrast, the Trk receptor inhibitor k-252a increased spine density by itself, and prevented BDNF from further increasing spine density. However, most of the spines in k-252a-treated slices were of the immature type. These effects of k-252a on spine density and morphology required neuronal activity because they were prevented by TTX. These divergent BDNF actions on spine density and morphology are reminiscent of opposing functional signaling by p75(NTR) and Trk receptors and reveal an unexpected level of complexity in the consequences of BDNF signaling on dendritic morphology.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.