ArticlePloS one2015
The transfection of BDNF to dopamine neurons potentiates the effect of dopamine D3 receptor agonist recovering the striatal innervation, dendritic spines and motor behavior in an aged rat model of Parkinson's disease.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.
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Who cites it
38 citing papers in PubMed, 1 synthesis or guideline pooled it, 89 citations in OpenAlex.
- Brain Derived Neurotrophic Factor and Cognitive Dysfunction in the Schizophrenia-Bipolar Spectrum: A Systematic Review and Meta-Analysis.Frontiers in psychiatry · 2022Pooled it
- Castration-induced nigrostriatal deficits are linked to reduced TrkB and loss of mature spines in the dorsal striatum.Frontiers in endocrinology · 2026Article
- SU-Eohyeol Pharmacopuncture Ameliorates Parkinson's Disease-Associated Pain via the CB1 and PPARγ Pathways in an MPTP-Induced Mouse Model.Pain research & management · 2026Article
- TLR3 activation in astrocytes attenuates the nigrostriatal pathway degeneration in rodent models of Parkinson's disease.Frontiers in cellular neuroscience · 2026Article
- Effects of traditional Chinese exercises on brain-derived neurotrophic factor in middle-aged and older adults: A systematic review and meta-analysis of randomized controlled trials.Journal of exercise science and fitness · 2025Review
- Focused ultrasound on the substantia nigra enables safe neurotensin-polyplex nanoparticle-mediated gene delivery to dopaminergic neurons intranasally and by blood circulation.Discover nano · 2024Article
- Transfection of the BDNF Gene in the Surviving Dopamine Neurons in Conjunction with Continuous Administration of Pramipexole Restores Normal Motor Behavior in a Bilateral Rat Model of Parkinson's Disease.Parkinson's disease · 2024Article
- Dimethyl fumarate abrogates striatal endoplasmic reticulum stress in experimentally induced late-stage Huntington's disease: Focus on the IRE1α/JNK and PERK/CHOP trajectories.Frontiers in pharmacology · 2023Article
- BDNF Val66Met Polymorphism: Suggested Genetic Involvement in Some Children with Learning Disorder.Journal of molecular neuroscience : MN · 2023Article
- Article
- BDNF Therapeutic Mechanisms in Neuropsychiatric Disorders.International journal of molecular sciences · 2022Review
- New Frontiers in Neurodegeneration and Regeneration Associated with Brain-Derived Neurotrophic Factor and the rs6265 Single Nucleotide Polymorphism.International journal of molecular sciences · 2022Review
- Cerebral dopamine neurotrophic factor transfection in dopamine neurons using neurotensin-polyplex nanoparticles reverses 6-hydroxydopamine-induced nigrostriatal neurodegeneration.Neural regeneration research · 2022Article
- Review
- A retrospective evaluation of the Brain and Body Fitness Studio service on functional capacity and quality of life in people with neurological disorders.Frontiers in neurology · 2022Article
- Review
- Adult Endogenous Dopaminergic Neuroregeneration Against Parkinson's Disease: Ideal Animal Models?Neurotoxicity research · 2021Review
- The BDNF Val66Met polymorphism (rs6265) enhances dopamine neuron graft efficacy and side-effect liability in rs6265 knock-in rats.Neurobiology of disease · 2021Article
- The Relation of the Brain-Derived Neurotrophic Factor with MicroRNAs in Neurodegenerative Diseases and Ischemic Stroke.Molecular neurobiology · 2021Review
- Exercise-Induced Neuroprotection in the 6-Hydroxydopamine Parkinson's Disease Model.Neurotoxicity research · 2020Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
The progressive degeneration of the dopamine neurons of the pars compacta of substantia nigra and the consequent loss of the dopamine innervation of the striatum leads to the impairment of motor behavior in Parkinson's disease. Accordingly, an efficient therapy of the disease should protect and regenerate the dopamine neurons of the substantia nigra and the dopamine innervation of the striatum. Nigral neurons express Brain Derived Neurotropic Factor (BDNF) and dopamine D3 receptors, both of which protect the dopamine neurons. The chronic activation of dopamine D3 receptors by their agonists, in addition, restores, in part, the dopamine innervation of the striatum. Here we explored whether the over-expression of BDNF by dopamine neurons potentiates the effect of the activation of D3 receptors restoring nigrostriatal innervation. Twelve-month old Wistar rats were unilaterally injected with 6-hydroxydopamine into the striatum. Five months later, rats were treated with the D3 agonist 7-hydroxy-N,N-di-n-propy1-2-aminotetralin (7-OH-DPAT) administered i.p. during 4½ months via osmotic pumps and the BDNF gene transfection into nigral cells using the neurotensin-polyplex nanovector (a non-viral transfection) that selectively transfect the dopamine neurons via the high-affinity neurotensin receptor expressed by these neurons. Two months after the withdrawal of 7-OH-DPAT when rats were aged (24 months old), immunohistochemistry assays were made. The over-expression of BDNF in rats receiving the D3 agonist normalized gait and motor coordination; in addition, it eliminated the muscle rigidity produced by the loss of dopamine. The recovery of motor behavior was associated with the recovery of the nigral neurons, the dopamine innervation of the striatum and of the number of dendritic spines of the striatal neurons. Thus, the over-expression of BDNF in dopamine neurons associated with the chronic activation of the D3 receptors appears to be a promising strategy for restoring dopamine neurons in Parkinson's disease.
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Registered trials
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