Session Time: 1:15pm-2:45pm
Location: Les Muses, Level 3
Objective: Analyzing the reserpine model of Parkinsonian syndrome
Background: There are several experimental models of Parkinson’s disease: reserpine, methamphetamine, 6-hydroxydopamine (6-OHDA), 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine – substances that selectively destroy catecholaminergic systems or disrupt their normal functioning. It has also been found that some agricultural chemicals, such as rotenone and paraquat, when administered systematically, can reproduce a number of key features of Parkinson’s disease in rodents.
Method: The reserpine model of Parkinson syndrome was achieved with a single injection of reserpine at a dose of 3 mg / kg subcutaneously. The work was carried out on male Wistar rats weighing 250-300 g. Reserpine was dissolved in glacial acetic acid (100 μl), then in water for injection at a ratio of 1: 35.
Results: After two hours of introduction of the toxin, the animals developed the following symptoms: rigidity, ptosis of the upper eyelid and tremor. Reserpine is a central sympatholytic, systemic administration of the drug depletes dopamine in the nerve endings and induces a hypokinetic state in rodents. Reserpine causes the release of other neurotransmitters that may not be directly involved in the molecular pathogenesis of Parkinson’s disease.
Conclusion: This model is suitable for studying the possibilities of correcting the pathology with the help of various pharmacological agents. Its advantage lies in the rapid development of Parkinson syndrome in experimental animals: the symptoms occur as early as 2 hours after the administration of the reserve and persist for up to 4 days. On this model, it is possible to study new drug anti-parkinsonian substances with their both systemic and intracerebral administration. The predictive value of testing for symptomatic drugs on the reserpine-induced model is low, since some drugs that reduce reserpine motor impairment are ineffective in Parkinson’s disease. However, such a model opens up opportunities for the creation and testing of new drug approaches aimed at reducing the cognitive deficit in Parkinson’s disease
To cite this abstract in AMA style:M. Tukhtamishev, F. Akhmedova. Experimental model of developing of Parkinson’s disease [abstract]. Mov Disord. 2019; 34 (suppl 2). https://www.mdsabstracts.org/abstract/experimental-model-of-developing-of-parkinsons-disease/. Accessed December 7, 2023.
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MDS Abstracts - https://www.mdsabstracts.org/abstract/experimental-model-of-developing-of-parkinsons-disease/