ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
The role of brain-derived neurotrophic factor (BDNF) in the development of neurogenic detrusor overactivity (NDO).
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 2 of them syntheses that pooled it.
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Who cites it
26 citing papers in PubMed, 2 syntheses or guidelines pooled it, 48 citations in OpenAlex.
- Molecular Mechanism Operating in Animal Models of Neurogenic Detrusor Overactivity: A Systematic Review Focusing on Bladder Dysfunction of Neurogenic Origin.International journal of molecular sciences · 2023Pooled it
- Association between Val66Met polymorphisms in brain-derived neurotrophic factor gene and asthma risk: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2015Pooled it
- Article
- A comprehensive visual report of urodynamic study in rats with spinal cord injury.Current urology · 2025Article
- Review
- Axonal growth inhibitors and their receptors in spinal cord injury: from biology to clinical translation.Neural regeneration research · 2023Review
- Molecular Mechanisms of Neurogenic Lower Urinary Tract Dysfunction after Spinal Cord Injury.International journal of molecular sciences · 2023Review
- Article
- Neurobiological insights into lower urinary tract dysfunction: evaluating the role of brain-derived neurotrophic factor.American journal of clinical and experimental urology · 2023Review
- Spinal Cord Injury Causes Marked Tissue Rearrangement in the Urethra-Experimental Study in the Rat.International journal of molecular sciences · 2022Article
- Development of Neurogenic Detrusor Overactivity after Thoracic Spinal Cord Injury Is Accompanied by Time-Dependent Changes in Lumbosacral Expression of Axonal Growth Regulators.International journal of molecular sciences · 2022Article
- Targeting neurotrophin and nitric oxide signaling to treat spinal cord injury and associated neurogenic bladder overactivity.Continence (Amsterdam, Netherlands) · 2022Article
- Vascular-Cognitive Impairment following High-Thoracic Spinal Cord Injury Is Associated with Structural and Functional Maladaptations in Cerebrovasculature.Journal of neurotrauma · 2020Article
- Effect of amniotic fluid stem cell transplantation on the recovery of bladder dysfunction in spinal cord-injured rats.Scientific reports · 2020Article
- BDNF promotes activation of astrocytes and microglia contributing to neuroinflammation and mechanical allodynia in cyclophosphamide-induced cystitis.Journal of neuroinflammation · 2020Article
- Partners in Crime: NGF and BDNF in Visceral Dysfunction.Current neuropharmacology · 2019Review
- Drug Targets in Neurotrophin Signaling in the Central and Peripheral Nervous System.Molecular neurobiology · 2018Review
- BDNF overexpression in the bladder induces neuronal changes to mediate bladder overactivity.American journal of physiology. Renal physiology · 2018Article
- Nerve growth factor-dependent hyperexcitability of capsaicin-sensitive bladder afferent neurones in mice with spinal cord injury.Experimental physiology · 2018Article
- Aberrant cortical thickness in neurologically asymptomatic patients with end-stage renal disease.Neuropsychiatric disease and treatment · 2018Article
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
Neurogenic detrusor overactivity (NDO) is a well known consequence of spinal cord injury (SCI), recognizable after spinal shock, during which the bladder is areflexic. NDO emergence and maintenance depend on profound plastic changes of the spinal neuronal pathways regulating bladder function. It is well known that neurotrophins (NTs) are major regulators of such changes. NGF is the best-studied NT in the bladder and its role in NDO has already been established. Another very abundant neurotrophin is BDNF. Despite being shown that, acting at the spinal cord level, BDNF is a key mediator of bladder dysfunction and pain during cystitis, it is presently unclear if it is also important for NDO. This study aimed to clarify this issue. Results obtained pinpoint BDNF as an important regulator of NDO appearance and maintenance. Spinal BDNF expression increased in a time-dependent manner together with NDO emergence. In chronic SCI rats, BDNF sequestration improved bladder function, indicating that, at later stages, BDNF contributes NDO maintenance. During spinal shock, BDNF sequestration resulted in early development of bladder hyperactivity, accompanied by increased axonal growth of calcitonin gene-related peptide-labeled fibers in the dorsal horn. Chronic BDNF administration inhibited the emergence of NDO, together with reduction of axonal growth, suggesting that BDNF may have a crucial role in bladder function after SCI via inhibition of neuronal sprouting. These findings highlight the role of BDNF in NDO and may provide a significant contribution to create more efficient therapies to manage SCI patients.
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