ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Rescue of mesencephalic dopaminergic neurons in culture by low-level stimulation of voltage-gated sodium channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 116 citations in OpenAlex.
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- The potential role and mechanism of Rhizoma Coptidis in prevention of diabetic encephalopathy: targeting sodium ion and channels.Frontiers in pharmacology · 2025Article
- Strategies targeting endoplasmic reticulum stress to improve Parkinson's disease.Frontiers in pharmacology · 2023Review
- The Common Cellular Events in the Neurodegenerative Diseases and the Associated Role of Endoplasmic Reticulum Stress.International journal of molecular sciences · 2022Review
- Effect of Acupuncture on Movement Function in Patients with Parkinson's Disease: Network Meta-Analysis of Randomized Controlled Trials.Healthcare (Basel, Switzerland) · 2021Article
- Apamin Enhances Neurite Outgrowth and Regeneration after Laceration Injury in Cortical Neurons.Toxins · 2021Article
- Physiology and Therapeutic Potential of SK, H, and M Medium AfterHyperPolarization Ion Channels.Frontiers in molecular neuroscience · 2021Review
- Venoms as an adjunctive therapy for Parkinson's disease: where are we now and where are we going?Future science OA · 2020Review
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- Dopamine neuronal protection in the mouse Substantia nigra by GHSR is independent of electric activity.Molecular metabolism · 2019Article
- Novel Approaches for the Treatment of Alzheimer's and Parkinson's Disease.International journal of molecular sciences · 2019Review
- Electrophysiological evidence of RML12 mosquito cell line towards neuronal differentiation by 20-hydroxyecdysdone.Scientific reports · 2018Article
- Potassium Channels: A Potential Therapeutic Target for Parkinson's Disease.Neuroscience bulletin · 2018Review
- Animal Toxins as Therapeutic Tools to Treat Neurodegenerative Diseases.Frontiers in pharmacology · 2018Review
- A Subpopulation of Dopaminergic Neurons Coexpresses Serotonin in Ventral Mesencephalic Cultures But Not After Intrastriatal Transplantation in a Rat Model of Parkinson's Disease.Cell transplantation · 2017Article
- Optogenetic Rescue of Locomotor Dysfunction and Dopaminergic Degeneration Caused by Alpha-Synuclein and EKO Genes.Experimental neurobiology · 2017Article
- The multi-target effects of CNI-1493: convergence of anti-amylodogenic and anti-inflammatory properties in animal models of Alzheimer's disease.Molecular medicine (Cambridge, Mass.) · 2016Article
- Converging roles of ion channels, calcium, metabolic stress, and activity pattern of Substantia nigra dopaminergic neurons in health and Parkinson's disease.Journal of neurochemistry · 2016Review
- Investigation of the effects of GABA receptor agonists in the differentiation of human induced pluripotent stem cells into dopaminergic neurons.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sections · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We used a model system in which dopaminergic (DA) neurons from embryonic rat mesencephalon undergo spontaneous and selective degeneration as they develop in culture. Here, we show that DA cell loss can be prevented efficiently by low concentrations of the Na+ channel agonist veratridine. The survival promoting effect of veratridine was reproduced by, but independent of, glial cell line-derived neurotrophic factor. Neuroprotection by veratridine was exquisitely specific to DA neurons, short-lived after withdrawal, and abolished by tetrodotoxin, indicating that activation of voltage-gated Na+ channels was crucially involved. Calcium measurements showed that veratridine-induced Na+ influx was necessary to maintain intracellular Ca2+ within a neuroprotective range through the stimulation of low-voltage activated T-type calcium channels, a mechanism that was distinct from that elicited by high K+-evoked depolarization. Interestingly, increasing neuronal excitability by treatment with apamin, an inhibitor of Ca2+-activated K+ channels, or with ouabain, a blocker of the Na+/K+-ATPase pump, was also neuroprotective by a mechanism involving T-type calcium channel activation. These results support the idea that mesencephalic DA neurons depend primarily on excitatory input for their survival during development.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.