ArticleInternational neurourology journal2022
Changes in the Neuronal Architecture of the Hippocampus in a 6-Hydroxydopamine-Lesioned Rat Model of Parkinson Disease.
Article in International neurourology journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers, 1 of them a synthesis that pooled it.
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Who cites it
12 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Challenges and Opportunities in Exploring Non-Motor Symptoms in 6-Hydroxydopamine Models of Parkinson's Disease: A Systematic Review.Journal of neurochemistry · 2025Pooled it
- Olfactory bulb 6-OHDA neurotoxicity as a model of early cortical dysfunction.Molecular and cellular biochemistry · 2026Article
- Article
- Molecular Pathogenesis of Memory Impairment in Parkinson's Disease: An Exploration of Underlying Mechanisms.Health science reports · 2026Article
- Synergistic Effects of Levodopa, Benserazide, and Nortriptyline on Behavioral Impairments and Brain Pathology in an Experimental Rat Model of Parkinson's Disease.Neurology research international · 2026Article
- Curcumin treatment reduces motor impairments and protects against rotenone-induced neurodegeneration in a rat model of Parkinson disease.Metabolic brain disease · 2025Article
- Changes in structural plasticity of hippocampal neurons in an animal model of multiple sclerosis.Zoological research · 2024Article
- Understanding the spectrum of non-motor symptoms in multiple sclerosis: insights from animal models.Neural regeneration research · 2024Review
- Identifying candidate genes associated with hippocampal dysfunction in a hemiparkinsonian rat model by transcriptomic profiling.Animal cells and systems · 2024Article
- Dopamine depletion alters neuroplasticity-related signaling in the rat hippocampus.Animal cells and systems · 2023Article
- Looking Forward to Saying Goodbye to COVID-19 and a Step Forward.International neurourology journal · 2022Article
- Epigenetic Dysfunction of Neurodegenerative Diseases, MeCP2 and More.International neurourology journal · 2022Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
purposeParkinson disease (PD) is a progressive neurodegenerative disorder in which dopaminergic (DAergic) systems are destroyed (particularly in the nigrostriatal system), causing both motor and nonmotor symptoms. Hippocampal neuroplasticity is altered in PD animal models, resulting in nonmotor dysfunctions. However, little is known about the precise mechanism underlying the hippocampal dysfunctions in PD.
methodsStriatal 6-hydroxydopamine (6-OHDA) infusions were performed unilaterally in adult Sprague Dawley rats. Both motor and nonmotor symptoms alongside the expression of tyrosine hydroxylase (TH) in the substantia nigra and striatum were confirmed in 6-OHDA-lesioned rats. The neuronal architecture in the hippocampus was analyzed by Golgi staining.
resultsDuring the 7-8 weeks after infusion, the 6-OHDA-lesioned rats exhibited motor and nonmotor dysfunctions (especially anxiety/depression-like behaviors). Rats with unilateral 6-OHDA infusion displayed reduced TH+ immunoreactivity in the ipsilateral nigrostriatal pathway of the brain. Golgi staining revealed that striatal 6-OHDA infusion significantly decreased the dendritic complexity (i.e., number of crossing dendrites, total dendritic length, and branch points) in the ipsilateral hippocampal conus ammonis 1 (CA1) apical/basal and dentate gyrus (DG) subregions. Additionally, the dendritic spine density and morphology were significantly altered in the CA1 apical/basal and DG subregions following striatal 6-OHDA infusion. However, alteration of microglial and astrocytic distributions did not occur in the hippocampus following striatal 6-OHDA infusion.
conclusionThe present study provides anatomical evidence that the structural plasticity in the hippocampus is altered in the late phase following striatal 6-OHDA infusion in rats, possibly as a result of the prolonged suppression of the DAergic system, and independent of neuroinflammation.
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