ArticleBrain sciences2022
Changes in Tyrosine Hydroxylase Activity and Dopamine Synthesis in the Nigrostriatal System of Mice in an Acute Model of Parkinson's Disease as a Manifestation of Neurodegeneration and Neuroplasticity.
Article in Brain sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 21 citations in OpenAlex.
- O-GlcNAcylation: A molecular switch linking brain health to neurodegeneration.Neural regeneration research · 2026Article
- Reimagining the contribution of iron in Parkinson's disease.Neurobiology of disease · 2026Review
- Preservation of Extracellular and Tissue Dopamine During Tyrosine Hydroxylase Loss in Rat 6-OHDA Parkinson's Model: Selective Compensation Restricted to Substantia Nigra.International journal of molecular sciences · 2026Article
- Modulation of Oxidative Stress and Apoptosis by Antrodia cinnamomea-Loaded Citrate-Stabilized Silver Nanoparticles in Experimental Parkinsonism.Molecular neurobiology · 2026Article
- Article
- Methamphetamine-Driven Neuroinflammation and Parkinson's Disease Pathology: Mechanistic Insight into Nrf2 and NFĸB Signaling.Molecular neurobiology · 2026Review
- Beyond Organ Boundaries: Molecular Mechanisms of Hepatic Encephalopathy and Parkinson's Disease from the Perspective of the Gut-Liver-Brain Axis.Research (Washington, D.C.) · 2026Review
- Artificial intelligence empowers gut microbiota research in neurodegenerative diseases molecular mechanisms and precision therapy.iScience · 2025Review
- Early α-Synuclein Pathology Induces Neuroinflammation and Decreases Topoisomerase IIβ Expression in A53T Mice.Inflammation · 2025Article
- The role of gasotransmitters in Parkinson's disease: Interplay of nitric oxide, carbon monoxide, and hydrogen sulfide.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Review
- TUDCA combined with Syndopa protects the midbrain and gut from MPTP toxicity in a Parkinson's disease mouse model: Immunohistochemical evidence.Biomolecules & biomedicine · 2025Article
- Initial Molecular Mechanisms of the Pathogenesis of Parkinson's Disease in a Mouse Neurotoxic Model of the Earliest Preclinical Stage of This Disease.International journal of molecular sciences · 2024Article
- Dopamine Signaling in Substantia Nigra and Its Impact on Locomotor Function-Not a New Concept, but Neglected Reality.International journal of molecular sciences · 2024Review
- Chronic Ultrasound Prenatal Stress Altered the Brain's Neurochemical Systems in Newborn Rats.Neural plasticity · 2024Article
- Article
- The Gene Expression of Proteins Involved in Intercellular Signaling and Neurodegeneration in the Substantia Nigra in a Mouse Subchronic Model of Parkinson's Disease.International journal of molecular sciences · 2023Article
- Retinal alpha-synuclein accumulation correlates with retinal dysfunction and structural thinning in the A53T mouse model of Parkinson's disease.Frontiers in neuroscience · 2023Article
- New Insights into Molecular Mechanisms Underlying Neurodegenerative Disorders.Brain sciences · 2022Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The progressive degradation of the nigrostriatal system leads to the development of Parkinson's disease (PD). The synthesis of dopamine, the neurotransmitter of the nigrostriatal system, depends on the rate-limiting enzyme, tyrosine hydroxylase (TH). In this study, we evaluated the synthesis of dopamine during periods of neurodegradation and neuroplasticity in the nigrostriatal system on a model of the early clinical stage of PD. It was shown that the concentration of dopamine correlated with activity of TH, while TH activity did not depend on total protein content either in the SN or in the striatum. Both during the period of neurodegeneration and neuroplasticity, TH activity in SN was determined by the content of P19-TH, and in the striatum it was determined by P31-TH and P40-TH (to a lesser extent). The data obtained indicate a difference in the regulation of dopamine synthesis between DA-neuron bodies and their axons, which must be considered for the further development of symptomatic pharmacotherapy aimed at increasing TH activity.
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