BDNF effects on dendritic spine morphology and hippocampal function
Abstract
Neurotrophins, including brain-derived neurotrophic factor (BDNF), are expressed in the hippocampus, as well as their precursors, the pro-neurotrophins. The neurotrophins signal through specific tyrosine kinase receptors and the low affinity receptor p75NTR. Moreover, the pro-neurotrophins are considered to be biologically active by signaling through specific receptors. The neurotrophins, especially BDNF, are involved in processes related to learning and memory. Furthermore, it is thought that BDNF also plays a crucial role in major depression. This points to a role of BDNF as a central regulator of neuronal plasticity within the postnatal hippocampus. Morphological correlates of neuronal plasticity are changes on the level of the dendritic spines and, at least in the dentate gyrus of the hippocampus, on the level of adult neurogenesis. Specific changes in dendritic spines as well as in adult hippocampal neurogenesis can be seen in the context of several forms of learning and memory, and it is known that depression is accompanied by declines in the rate of adult neurogenesis and in spine densities. The possible roles of BDNF in neuronal plasticity within the hippocampus are highlighted in this review by focusing on the morphological components of neuronal plasticity.
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Hippocampal volume is linked to BDNF-mediated TrkB signaling.
“suggesting a link between hippocampal volume and BDNF-mediated TrkB signaling (von Bohlen und Halbach et al. 2003; von Bohlen Und Halbach and von Bohlen Und Halbach 2018).”
From Neurotrophic factors and neuroplasticity pathways in the pathophysiology and treatment of depression (2018) · cites this paper as von Bohlen Und Halbach and von Bohlen Und Halbach 2018
Heterozygous BDNF mice display a specific hippocampal volume reduction similar to that observed in heterozygous TrkB mice, but in contrast to p75NTR-deficient mice.
“At morphological level, these mice display a specific hippocampal volume reduction [180] similar to that observed in heterozygous TrkB mice [181,182], but in contrast to p75NTR-deficient mice [183].”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [181]
These findings suggest a link between hippocampal volume and BDNF-mediated TrkB signaling.
“These findings suggest a link between hippocampal volume and BDNF-mediated TrkB signaling [181,182].”
From Neurotrophic Factor BDNF, Physiological Functions and Therapeutic Potential in Depression, Neurodegeneration and Brain Cancer (2020) · cites this paper as [181]
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- Authors
- von Bohlen und Halbach, O., & von Bohlen und Halbach, V.
- Venue
- Cell and Tissue Research
- Published
- 2018-02-15
- Volume
- 373
- Issue
- 3
- Pages
- 729-741
- ISSN
- 0302-766X (ISSN-L)
- 1432-0878
- OpenAlex
- W2788533076
- Cited by
- 218
- References
- 15
- Citations by year
- 2026: 15 · 2025: 20 · 2024: 26 · 2023: 41 · 2022: 37 · 2021: 30 · 2020: 29 · 2019: 16 · 2018: 4
- FWCI
- 2.56
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Cell and Tissue Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- brain-derived neurotrophic factor, dendritic spine morphology, hippocampus, adult neurogenesis, dentate gyrus, neuroplasticity, neurotrophins, p75 neurotrophin receptor, receptor tyrosine kinase, learning and memory, depression
- MeSH terms
- Animals, Hippocampus, Humans, Mice, Transgenic, Neuronal Plasticity, Neurons, Polymorphism, Genetic, Synapses, Long-Term Potentiation, Mice, Knockout, Brain-Derived Neurotrophic Factor, Long-Term Synaptic Depression, Dendritic Spines, Mice, Rats
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