The DOI matches its Crossref record; 245 of the 246 references it cites were found in a registry or an index.
Pre- and postsynaptic twists in BDNF secretion and action in synaptic plasticity.
Abstract
Overwhelming evidence collected since the early 1990's strongly supports the notion that BDNF is among the key regulators of synaptic plasticity in many areas of the mammalian central nervous system. Still, due to the extremely low expression levels of endogenous BDNF in most brain areas, surprisingly little data i) pinpointing pre- and postsynaptic release sites, ii) unraveling the time course of release, and iii) elucidating the physiological levels of synaptic activity driving this secretion are available. Likewise, our knowledge regarding pre- and postsynaptic effects of endogenous BDNF at the single cell level in mediating long-term potentiation still is sparse. Thus, our review will discuss the data currently available regarding synaptic BDNF secretion in response to physiologically relevant levels of activity, and will discuss how endogenously secreted BDNF affects synaptic plasticity, giving a special focus on spike timing-dependent types of LTP and on mossy fiber LTP. We will attempt to open up perspectives how the remaining challenging questions regarding synaptic BDNF release and action might be addressed by future experiments. This article is part of the Special Issue entitled 'BDNF Regulation of Synaptic Structure, Function, and Plasticity'.
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In the citing paper
“Especially in the hippocampus, this neurotrophin is thought to act on both the pre- and post-synaptic compartments, modulating synaptic efficacy, either by changing the pre-synaptic transmitter release, or by increasing post-synaptic transmitter sensitivity [15,16] to induce a long-lasting increase in synaptic plasticity.”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [16]
In the citing paper
“The effects of BDNF on LTP are mediated by the TrkB receptor.”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [16]
In the citing paper
“In addition, studies also show that BDNF is an important regulator of synaptic transmission and long-term potentiation (LTP) in the hippocampus and in other brain regions.”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [16]
In the citing paper
“In particular, in the hippocampus the neurotrophin is thought to act at pre- and post-synaptic levels, modulating synaptic efficacy either by changes in pre-synaptic transmitter release, or by increased post-synaptic transmitter sensitivity (see e.g., [15,16]) to induce a long-lasting increase in synaptic plasticity.”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [16]
In the citing paper
“The protein is thought to interact with energy metabolism to facilitate both pre- and post-synaptic mechanisms and the induction of LTP (Gomez-Pinilla and Hillman, 2013; Edelmann et al., 2014), as well as promoting the proliferation and survival of adult-born granule cells (Korol et al., 2013; Park and Poo, 2013).”
From Aerobic Exercise as a Tool to Improve Hippocampal Plasticity and Function in Humans: Practical Implications for Mental Health Treatment (2016) · cites this paper as Edelmann et al., 2014
In the citing paper
“In the brain, BDNF is involved in plasticity, neuronal survival, formation of new synapses, dendritic branching, and modulation of excitatory and inhibitory neurotransmitter profiles [11, 12].”
From Brain-Derived Neurotrophic Factor in Brain Disorders: Focus on Neuroinflammation (2019) · cites this paper as [11]
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Metadata
- Authors
- Edelmann, E., Leßmann, V., & Brigadski, T.
- Affiliations
- Otto-von-Guericke-Universität Magdeburg (DE)
- Center for Behavioral Brain Sciences (DE)
- Corresponding author
- Leßmann, Volkmar
- Venue
- Neuropharmacology
- Publisher
- Elsevier BV
- Published
- 2014-01
- Volume
- 76
- Pages
- 610-627
- ISSN
- 0028-3908 (ISSN-L)
- OpenAlex
- W1973883693
- Cited by
- 248
- References
- 246
- Citations by year
- 2026: 9 · 2025: 10 · 2024: 23 · 2023: 23 · 2022: 19 · 2021: 24 · 2020: 18 · 2019: 22 · 2018: 23 · 2017: 20 · 2016: 24 · 2015: 12 · 2014: 14
- FWCI
- 1.93
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuropharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- brain-derived neurotrophic factor, BDNF secretion, synaptic plasticity, long-term potentiation, spike-timing-dependent plasticity, presynaptic neurotransmitter release, postsynaptic effects, central nervous system
- MeSH terms
- Animals, Neuronal Plasticity, Presynaptic Terminals, Brain-Derived Neurotrophic Factor, Post-Synaptic Density
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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