Degeneration of nigrostriatal dopaminergic neurons in an experimental model of the early clinical stage of Parkinson’s disease

Колачева, А. А.; Козина, Е. А.; Volina, E. V.; Ugryumov, M. V.

doi:10.1134/s1819712414030076

Cited by 5 publications

(4 citation statements)

References 28 publications

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“…Previously, we demonstrated that degeneration of DA-ergic axonal terminals in the striatum stops 6 h after four MPTP injections, after which compensatory processes begin to develop (e.g., an increase in the TH activity) [ 7 ]. The number of axonal terminals after 3 and 6 h was 67 and 55% of the control value, respectively [ 7 ]. In this period, the rate of axonal terminal degeneration within the first hour was 4%.…”

Section: Resultsmentioning

confidence: 99%

“…1A ). Tyrosine hydroxylase (TH) ( n = 3–4) in striatal slices was detected by immunohistochemistry (IHC), followed by the counting of axonal terminals in four areas of the dorsal striatum as described previously [ 7 ]. Also, the striatal DA concentration was determined by high-performance liquid chromatography with electrochemical detection (HPLC-ED) ( n = 5–7) ( Fig.…”

Section: Methodsmentioning

confidence: 99%

“…Also, the nomifensine experiment included a quantification of TH-immunoreactive axonal terminals in the striatum. Details of the procedures for immunohistochemical detection of TH, counting of axonal terminals, and measuring of the striatal DA concentration are described elsewhere [ 7 ].…”

Section: Methodsmentioning

confidence: 99%

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A Mouse Model of Nigrostriatal Dopaminergic Axonal Degeneration As a Tool for Testing Neuroprotectors

Колачева

Ugrumov

2021

Acta Naturae

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Degeneration of nigrostriatal dopaminergic neurons in Parkinsons disease begins from the axonal terminals in the striatum and, then, in retrograde fashion, progresses to the cell bodies in the substantia nigra. Investigation of the dynamics of axonal terminal degeneration may help in the identification of new targets for neuroprotective treatment and be used as a tool for testing potential drugs. We have shown that the degeneration rate of dopaminergic axonal terminals changes over time, and that the striatal dopamine concentration is the most sensitive parameter to the action of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). This model was validated using neuroprotectors with well-known mechanisms of action: the dopamine transporter inhibitor nomifensine and SEMAX peptide that stimulates the secretion of endogenous neurotrophic factors or acts as an antioxidant. Nomifensine was shown to almost completely protect dopaminergic fibers from the toxic effect of MPTP and maintain the striatal dopamine concentration at the control level. However, SEMAX, slightly but reliably, increased striatal dopamine when administered before MPTP treatment, which indicates that it is more effective as an inductor of endogenous neurotrophic factor secretion rather than as an antioxidant.

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Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

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A Mouse Model of Nigrostriatal Dopaminergic Axonal Degeneration As a Tool for Testing Neuroprotectors

Колачева

Ugrumov

2021

Acta Naturae

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“…Недавно нами впервые была создана тест-система для поиска лекарственных веществ с нейропротективными свойствами на основе оригинальной модели ранней клинической стадии БП (мыши, МФТП) [138,139]. На этой модели впервые была определена динамика деградации нигростриарных дофаминергических нейронов -отдельно тел нейронов в черной субстанции и аксонов в стриатуме, в ответ на системное введение МФТП.…”

Section: разработка превентивной терапии на доклинической стадии ндзunclassified

Development of preclinical diagnosis and preventive treatment of neurodegenerative diseases

2015

Z. nevrol. psikhiatr. im. S.S. Korsakova

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Neurodegenerative diseases (NDD) are serious fatal neurological and mental diseases that resulted in disability and fethal outcome. Based on the advances of basic sciences over the last two decades, new knowledge on the risk factors for NDD and molecular mechanisms of the pathogenesis are obtained. It has been shown that the accelerated process of neuronal death which is the main cause of NDD development begins long before the appearance of clinical symptoms. The first symptoms appeared only after the death of most specific regulatory neurons and exhaustion of brain compensatory reserve. Only at that time, one can make the diagnosis and start traditional treatment of patients that accounts for the extremely low efficacy of the latter. Currently, complex preclinical diagnosis based on the identification of relatively specific clinical precursors and peripheral biomarkers has been developing. Development of preclinical diagnosis and preventive treatment is a strategic issue of modern neurology and psychiatry. The resolution of this issue allows to consider NDD as cured, but not fatal, diseases.

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Possible Involvement of Genes Related to Lysosomal Storage Disorders in the Pathogenesis of Parkinson’s Disease

et al. 2019

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Degeneration of nigrostriatal dopaminergic neurons in an experimental model of the early clinical stage of Parkinson’s disease

Cited by 5 publications

References 28 publications

A Mouse Model of Nigrostriatal Dopaminergic Axonal Degeneration As a Tool for Testing Neuroprotectors

A Mouse Model of Nigrostriatal Dopaminergic Axonal Degeneration As a Tool for Testing Neuroprotectors

Development of preclinical diagnosis and preventive treatment of neurodegenerative diseases

Possible Involvement of Genes Related to Lysosomal Storage Disorders in the Pathogenesis of Parkinson’s Disease

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