ArticleNeural plasticity2012
Intracellular Ca2+ stores and Ca2+ influx are both required for BDNF to rapidly increase quantal vesicular transmitter release.
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 30 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
30 citing papers in PubMed, 49 citations in OpenAlex.
- Indole-3-Carbinol and Its Derivatives as Neuroprotective Modulators.Brain sciences · 2024Review
- Muscarinic Receptors in Developmental Axonal Competition at the Neuromuscular Junction.Molecular neurobiology · 2023Article
- Several dementia subtypes and mild cognitive impairment share brain reduction of neurotransmitter precursor amino acids, impaired energy metabolism, and lipid hyperoxidation.Frontiers in aging neuroscience · 2023Article
- Brain-derived neurotrophic factor is a regulator of synaptic transmission in the adult visual thalamus.Journal of neurophysiology · 2022Article
- Presynaptic cGMP sets synaptic strength in the striatum and is important for motor learning.EMBO reports · 2022Article
- Brain Proteome and Behavioural Analysis in Wild Type, BDNFInternational journal of molecular sciences · 2022Article
- Synaptopathy Mechanisms in ALS Caused by C9orf72 Repeat Expansion.Frontiers in cellular neuroscience · 2021Article
- Ketamine and Calcium Signaling-A Crosstalk for Neuronal Physiology and Pathology.International journal of molecular sciences · 2020Review
- Myasthenia Gravis: From the Viewpoint of Pathogenicity Focusing on Acetylcholine Receptor Clustering, Trans-Synaptic Homeostasis and Synaptic Stability.Frontiers in molecular neuroscience · 2020Article
- Regulation of Acetylcholine Quantal Release by Coupled Thrombin/BDNF Signaling in Mouse Motor Synapses.Cells · 2019Article
- Article
- Endogenous cannabinoids mediate the effect of BDNF at CA1 inhibitory synapses in the hippocampus.Synapse (New York, N.Y.) · 2018Article
- A small-molecule TrkB ligand restores hippocampal synaptic plasticity and object location memory in Rett syndrome mice.Disease models & mechanisms · 2017Article
- Synaptic Homeostasis and Its Immunological Disturbance in Neuromuscular Junction Disorders.International journal of molecular sciences · 2017Review
- Presynaptic Membrane Receptors Modulate ACh Release, Axonal Competition and Synapse Elimination during Neuromuscular Junction Development.Frontiers in molecular neuroscience · 2017Review
- Presynaptic Muscarinic Acetylcholine Receptors and TrkB Receptor Cooperate in the Elimination of Redundant Motor Nerve Terminals during Development.Frontiers in aging neuroscience · 2017Article
- Calcium-Dependent and Synapsin-Dependent Pathways for the Presynaptic Actions of BDNF.Frontiers in cellular neuroscience · 2017Article
- TheFrontiers in cellular neuroscience · 2017Article
- Mechanisms of BDNF regulation in asthmatic airway smooth muscle.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) is well known as a survival factor during brain development as well as a regulator of adult synaptic plasticity. One potential mechanism to initiate BDNF actions is through its modulation of quantal presynaptic transmitter release. In response to local BDNF application to CA1 pyramidal neurons, the frequency of miniature excitatory postsynaptic currents (mEPSC) increased significantly within 30 seconds; mEPSC amplitude and kinetics were unchanged. This effect was mediated via TrkB receptor activation and required both full intracellular Ca(2+) stores as well as extracellular Ca(2+). Consistent with a role of Ca(2+)-permeable plasma membrane channels of the TRPC family, the inhibitor SKF96365 prevented the BDNF-induced increase in mEPSC frequency. Furthermore, labeling presynaptic terminals with amphipathic styryl dyes and then monitoring their post-BDNF destaining in slice cultures by multiphoton excitation microscopy revealed that the increase in frequency of mEPSCs reflects vesicular fusion events. Indeed, BDNF application to CA3-CA1 synapses in TTX rapidly enhanced FM1-43 or FM2-10 destaining with a time course that paralleled the phase of increased mEPSC frequency. We conclude that BDNF increases mEPSC frequency by boosting vesicular fusion through a presynaptic, Ca(2+)-dependent mechanism involving TrkB receptors, Ca(2+) stores, and TRPC channels.
Indexed as
Identifiers
What 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.