ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Endogenous truncated TrkB.T1 receptor regulates neuronal complexity and TrkB kinase receptor function in vivo.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers, 1 of them a synthesis that pooled it.
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Who cites it
75 citing papers in PubMed, 1 synthesis or guideline pooled it, 146 citations in OpenAlex.
- TrkB Truncated Isoform Receptors as Transducers and Determinants of BDNF Functions.Frontiers in neuroscience · 2022Pooled it
- Impact of Relapse in BDNF Receptors Expression in Patients With a First Episode of Schizophrenia.Schizophrenia bulletin · 2025Article
- A neurotrophin functioning with a Toll regulates structural plasticity in a dopaminergic circuit.eLife · 2024Article
- Genetic Variations in TrkB.T1 Isoform and Their Association With Somatic and Psychological Symptoms in Individuals With IBS.The journal of pain · 2024Article
- Review
- Memory-related hippocampal brain-derived neurotrophic factor activation pathways from repetitive transcranial magnetic stimulation in the 3xTg-AD mouse line.Experimental gerontology · 2023Article
- A Truncated Receptor TrkB Isoform (TrkB.T1) in Mechanisms of Genetically Determined Depressive-like Behavior of Mice.Biomedicines · 2023Article
- Activation of TrkB signaling mitigates cerebellar anomalies caused by Rbm4-Bdnf deficiency.Communications biology · 2023Article
- Article
- Hypothalamic TrkB.FL overexpression improves metabolic outcomes in the BTBR mouse model of autism.PloS one · 2023Article
- Oncogenic role of a developmentally regulatedScience advances · 2022Article
- BDNF Therapeutic Mechanisms in Neuropsychiatric Disorders.International journal of molecular sciences · 2022Review
- Astrocytic BDNF signaling within the ventromedial hypothalamus regulates energy homeostasis.Nature metabolism · 2022Article
- Counteracting epigenetic mechanisms regulate the structural development of neuronal circuitry in human neurons.Molecular psychiatry · 2022Article
- Transactivation of TrkB Receptors by Oxytocin and Its G Protein-Coupled Receptor.Frontiers in molecular neuroscience · 2022Article
- Neuroinflammation as the Underlying Mechanism of Postoperative Cognitive Dysfunction and Therapeutic Strategies.Frontiers in cellular neuroscience · 2022Review
- Music-Based Intervention AmelioratesInternational journal of molecular sciences · 2021Article
- Delayed onset of inherited ALS by deletion of the BDNF receptor TrkB.T1 is non-cell autonomous.Experimental neurology · 2021Article
- Adenosine ATranslational psychiatry · 2021Article
- A kinase-deficient NTRK2 splice variant predominates in glioma and amplifies several oncogenic signaling pathways.Nature communications · 2020Article
15 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 4 institutions in 2 countries.
Funding
Abstract
Pathological or in vitro overexpression of the truncated TrkB (TrkB.T1) receptor inhibits signaling through the full-length TrkB (TrkB.FL) tyrosine kinase receptor. However, to date, the role of endogenous TrkB.T1 is still unknown. By studying mice lacking the truncated TrkB.T1 isoform but retaining normal spatiotemporal expression of TrkB.FL, we have analyzed TrkB.T1-specific physiological functions and its effect on endogenous TrkB kinase signaling in vivo. We found that TrkB.T1-deficient mice develop normally but show increased anxiety in association with morphological abnormalities in the length and complexity of neurites of neurons in the basolateral amygdala. However, no behavioral abnormalities were detected in hippocampal-dependent memory tasks, which correlated with lack of any obvious hippocampal morphological deficits or alterations in basal synaptic transmission and long-term potentiation. In vivo reduction of TrkB signaling by removal of one BDNF allele could be partially rescued by TrkB.T1 deletion, which was revealed by an amelioration of the enhanced aggression and weight gain associated with BDNF haploinsufficiency. Our results suggest that, at the physiological level, TrkB.T1 receptors are important regulators of TrkB.FL signaling in vivo. Moreover, TrkB.T1 selectively affects dendrite complexity of certain neuronal populations.
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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.