The DOI matches its Crossref record; 222 of the 222 references it cites were found in a registry or an index.
Beyond good and evil: A putative continuum-sorting hypothesis for the functional role of proBDNF/BDNF-propeptide/mBDNF in antidepressant treatment
Open accessAbstract
Depression and posttraumatic stress disorder are assumed to be maladaptive responses to stress and antidepressants are thought to counteract such responses by increasing BDNF (brain-derived neurotrophic factor) levels. BDNF acts through TrkB (tropomyosin-related receptor kinase B) and plays a central role in neuroplasticity. In contrast, both precursor proBDNF and BDNF propeptide (another metabolic product from proBDNF cleavage) have a high affinity to p75 receptor (p75R) and usually convey apoptosis and neuronal shrinkage. Although BDNF and proBDNF/propeptide apparently act in opposite ways, neuronal turnover and remodeling might be a final common way that both act to promote more effective neuronal networking, avoiding neuronal redundancy and the misleading effects of environmental contingencies. This review aims to provide a brief overview about the BDNF functional role in antidepressant action and about p75R and TrkB signaling to introduce the "continuum-sorting hypothesis." The resulting hypothesis suggests that both BDNF/proBDNF and BDNF/propeptide act as protagonists to fine-tune antidepressant-dependent neuroplasticity in crucial brain structures to modulate behavioral responses to stress.
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“BDNF has been consistently associated to the therapeutic effect of antidepressant drugs [199,200,201].”
From P2X7 Receptor Signaling in Stress and Depression (2019) · cites this paper as [201]
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“Trk receptors are expressed by both motor neurons and skeletal myocytes, and their downstream signaling leads to the activation of PI3K, mitogen-activated protein kinase (MAPK), and phospholipase C-γ (PLCγ) pathways [89], ultimately supporting neuronal survival [91].”
BackgroundP2X7 Receptor Signaling in Stress and Depression
Ribeiro, D. E., Roncalho, A. L., Glaser, T., Ulrich, H., Wegener, G., & Joca, S. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20112778 · Cited by 129
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Metadata
- Authors
- Diniz, C. R. A. F., Casarotto, P. C., Resstel, L., & Joca, S. R. L.
- Affiliations
- Universidade de São Paulo (BR)
- University of Helsinki (FI)
- Corresponding author
- Diniz, Cassiano R.A.F.
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2018-07
- Volume
- 90
- Pages
- 70-83
- ISSN
- 0149-7634 (ISSN-L)
- OpenAlex
- W2795628695
- Semantic Scholar
- 901c33994c7064d67a1d28eaac7aa0969a073d89
- Cited by
- 58
- References
- 222
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 6 · 2023: 5 · 2022: 5 · 2021: 10 · 2020: 14 · 2019: 4 · 2018: 3
- FWCI
- 1.00
- Type
- journal article
- Language
- en
- Open access
- green
- hdl.handle.net
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Työväentutkimus Vuosikirja (submittedVersion)
- Funders
- Conselho Nacional de Desenvolvimento Científico e Tecnológico
- Fundação de Amparo à Pesquisa do Estado de São Paulo
- European Research Council
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nerve injury and regeneration
- Health Sciences › Medicine › Pharmacology (medical) › Treatment of Major Depression
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- brain-derived neurotrophic factor, proBDNF, antidepressant action, depression, post-traumatic stress disorder, TrkB signaling, p75 neurotrophin receptor, neuroplasticity, neuronal turnover, neuronal remodeling, stress response
- MeSH terms
- Antidepressive Agents, Brain, Depression, Neuronal Plasticity, Neurons, Brain-Derived Neurotrophic Factor
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