ArticleJournal of neurochemistry2009
Nicotine is neuroprotective when administered before but not after nigrostriatal damage in rats and monkeys.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
34 citing papers in PubMed, 93 citations in OpenAlex.
- Braking Parkinson's progression: the hypothetical druggable role of striatal parvalbumin interneurons.NPJ Parkinson's disease · 2026Review
- Proposed mechanisms of neuroprotection for nicotine in Parkinson's disease.Journal of Parkinson's disease · 2025Review
- Reorganization of Mitochondrial Function and Architecture in Response to Plant-Derived Alkaloids: Anatabine, Anabasine, and Nicotine, Investigated in SH-SY5Y Cells and in a Cellular Model of Parkinson's Disease.CNS neuroscience & therapeutics · 2025Article
- Using Constellation Pharmacology to Characterize a Novel α-Conotoxin fromMarine drugs · 2024Article
- Chronic Nicotine Consumption and Withdrawal Regulate Melanocortin Receptor, CRF, and CRF Receptor mRNA Levels in the Rat Brain.Brain sciences · 2024Article
- The double-edged nature of nicotine: toxicities and therapeutic potentials.Frontiers in pharmacology · 2024Review
- Nicotine-Mediated Recruitment of GABAergic Neurons to a Dopaminergic Phenotype Attenuates Motor Deficits in an Alpha-Synuclein Parkinson's Model.International journal of molecular sciences · 2023Article
- The protective role of cigarette smoking against Parkinson's disease via moderation of the interaction between iron deposition in the nigrostriatal pathway and clinical symptoms.Quantitative imaging in medicine and surgery · 2022Article
- Biologically Active Compounds Present in Tobacco Smoke: Potential Interactions Between Smoking and Mental Health.Frontiers in neuroscience · 2022Review
- Nicotine Has a Therapeutic Window of Effectiveness in aParkinson's disease · 2022Article
- Central Cholinergic Synapse Formation in Optimized Primary Septal-Hippocampal Co-cultures.Cellular and molecular neurobiology · 2021Article
- Interaction of Neuromelanin with Xenobiotics and Consequences for Neurodegeneration; Promising Experimental Models.Antioxidants (Basel, Switzerland) · 2021Review
- Article
- Cholinergic Receptor Modulation as a Target for Preventing Dementia in Parkinson's Disease.Frontiers in neuroscience · 2021Review
- Targeting the cholinergic system in Parkinson's disease.Acta pharmacologica Sinica · 2020Review
- Strategies for the Treatment of Parkinson's Disease: Beyond Dopamine.Frontiers in aging neuroscience · 2020Article
- Nicotine-induced dopamine plasticity: a gateway to neurotransmitter replacement?Neural regeneration research · 2020Article
- Nicotine-Induced Neuroprotection in Rotenone In Vivo and In Vitro Models of Parkinson's Disease: Evidences for the Involvement of the Labile Iron Pool Level as the Underlying Mechanism.Neurotoxicity research · 2019Article
- Dyskinesia and brain-derived neurotrophic factor levels after long-term levodopa and nicotinic receptor agonist treatments in female mice with near-total unilateral dopaminergic denervation.BMC neuroscience · 2018Article
- Saturation Binding of Nicotine to Synthetic Neuromelanin Demonstrated by Fluorescence Spectroscopy.Neurochemical research · 2016Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Nicotine reduces dopaminergic deficits in parkinsonian animals when administered before nigrostriatal damage. Here we tested whether nicotine is also beneficial when given to rats and monkeys with pre-existing nigrostriatal damage. Rats were administered nicotine before and after a unilateral 6-hydroxydopamine lesion of the medial forebrain bundle, and the results compared with those in which rats received nicotine only after lesioning. Nicotine pre-treatment attenuated behavioral deficits and lessened lesion-induced losses of the striatal dopamine transporter, and alpha6beta2* and alpha4beta2* nicotinic receptors (nAChRs). By contrast, nicotine administered 2 weeks after lesioning, when 6-hydroxydopamine-induced neurodegenerative effects are essentially complete, did not improve these same measures. Similar results were observed in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-lesioned monkeys. Nicotine did not enhance striatal markers when administered to monkeys with pre-existing nigrostriatal damage, in contrast to previous data that showed improvements when nicotine was given to monkeys before lesioning. These combined findings in two animal models suggest that nicotine is neuroprotective rather than neurorestorative against nigrostriatal damage. Receptor studies with (125)I-alpha-conotoxinMII and the alpha-conotoxinMII analog E11A were next performed to determine whether nicotine treatment pre- or post-lesioning differentially affected expression of alpha6alpha4beta2* and alpha6(nonalpha4)beta2* nAChR subtypes in striatum. The observations suggest that protection against nigrostriatal damage may be linked to striatal alpha6alpha4beta2* nAChRs.
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Registered trials
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.