ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2002
Brain-derived neurotrophic factor modulates cerebellar plasticity and synaptic ultrastructure.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
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The trial behind it
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Who cites it
89 citing papers in PubMed, 203 citations in OpenAlex.
- PTEN deficiency in postnatally developing Purkinje cells disrupts metabolic signaling, leading to dendritic abnormalities and sex-specific behavioral deficits.Scientific reports · 2025Article
- Effects of Qingyangshen glycosides on neuroplasticity in a mouse model of social defeat.Animal models and experimental medicine · 2025Article
- In Silico Analysis of miRNA-Regulated Pathways in Spinocerebellar Ataxia Type 7.Current issues in molecular biology · 2025Article
- Characterizing molecular and behavioral changes arising from ROMK potassium channel deficiency in the cerebellum.Frontiers in behavioral neuroscience · 2025Article
- Post-symptomatic administration of hMSCs exerts therapeutic effects in SCA2 mice.Stem cell research & therapy · 2024Article
- Mild repetitive TBI reduces brain-derived neurotrophic factor (BDNF) in the substantia nigra and hippocampus: A preclinical model for testing BDNF-targeted therapeutics.Experimental neurology · 2024Article
- Plasma and Platelet Brain-Derived Neurotrophic Factor (BDNF) Levels in Bipolar Disorder Patients with Post-Traumatic Stress Disorder (PTSD) or in a Major Depressive Episode Compared to Healthy Controls.International journal of molecular sciences · 2024Article
- Neuropeptides and Their Roles in the Cerebellum.International journal of molecular sciences · 2024Review
- BDNF and Cerebellar Ataxia.Current drug research reviews · 2024Review
- Reduced Cerebellar BDNF Availability Affects Postnatal Differentiation and Maturation of Granule Cells in a Mouse Model of Cholesterol Dyshomeostasis.Molecular neurobiology · 2023Article
- BDNF is altered in a brain-region specific manner and rescues deficits in Spinocerebellar Ataxia Type 1.Neurobiology of disease · 2023Article
- Mesenchymal Stem Cell Transplantation Ameliorates Ara-C-Induced Motor Deficits in a Mouse Model of Cerebellar Ataxia.Journal of clinical medicine · 2023Article
- Building better brains: the pleiotropic function of neurotrophic factors in postnatal cerebellar development.Frontiers in molecular neuroscience · 2023Review
- Cerebellum lineage allocation, morphogenesis and repair: impact of interplay amongst cells.Development (Cambridge, England) · 2022Review
- Selective activation and down-regulation of Trk receptors by neurotrophins in human neurons co-expressing TrkB and TrkC.Journal of neurochemistry · 2022Article
- Carotenoids from Marine Sources as a New Approach in Neuroplasticity Enhancement.International journal of molecular sciences · 2022Review
- Kidins220/ARMS modulates brain morphology and anxiety-like traits in adult mice.Cell death discovery · 2022Article
- The Role of Brain-Derived Neurotrophic Factor Signaling in Central Nervous System Disease Pathogenesis.Frontiers in human neuroscience · 2022Review
- How Are Adenosine and Adenosine ABiomedicines · 2021Review
- Review
29 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
4 authors at 3 institutions in 1 country.
Funding
Abstract
Neurotrophins are key regulators of neuronal survival and function. Here we show that TrkB, the receptor for brain-derived neurotrophic factor (BDNF), is located at parallel fiber to Purkinje cell (PF/PC) synapses of the cerebellum. To determine the effects of TrkB receptor activation on synapse formation and function, we examined the parallel fiber to Purkinje cell synapses of mice with a targeted deletion of the BDNF gene. Although Purkinje cell dendrites are abnormal in BDNF -/- mice, PF/PC synapses are still able to form. Immunohistochemical analysis of mutant animals revealed the formation of numerous PF/PC synapses with the appropriate apposition of presynaptic and postsynaptic proteins. These synapses are functional, and no differences were detected in the waveform of evoked EPSCs, the amplitude of spontaneous mini-EPSCs, or the response to prolonged 10 Hz stimulus trains. However, paired-pulse facilitation, a form of short-term plasticity, is significantly decreased in BDNF -/- mice. Detailed ultrastructural analysis of the presynaptic terminals demonstrated that this change in synaptic function is accompanied by an increase in the total number of synaptic vesicles in mutant mice and a decrease in the proportion of vesicles that are docked. These data suggest that BDNF regulates both the mechanisms that underlie short-term synaptic plasticity and the steady-state relationship between different vesicle pools within the terminal.
Indexed as
Identifiers
11850459PMC6757568W1796427658What OpenQuestion holds
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.