N. R. Tiras, I. Mikheeva, Gulnara Mihailova, N. Penkova, Sergey Surenovich Khutzian
{"title":"左旋多巴的使用诱导毛特纳神经元抵抗-淀粉样蛋白的神经毒性作用","authors":"N. R. Tiras, I. Mikheeva, Gulnara Mihailova, N. Penkova, Sergey Surenovich Khutzian","doi":"10.17816/morph.89904","DOIUrl":null,"url":null,"abstract":"Objective - to study the three-dimensional structure of Mauthner neurons in goldfish and the ultrastructure of their afferent synapses under the influence of L-dopa and the toxic fragment of 25-35 beta-amyloid.Materials and methods. The study was performed on Mauthner neurons of the goldfish fry (n=12) by the methods of light and electron microscopy. The identification of Mauthner's neurons and the reconstruction of their integral structure, the determination of the volume of the soma, ventral and lateral dendrites and the study of the structure of afferent synapses were carried out using serial sections 3 m thick.Results. The use of L-dopa stabilizes the size of the soma and ventral dendrites. A decrease in the volume of the lateral dendrite is accompanied either by an increase in the volume of its branches under the action of beta-amyloid, then L-dopa, or an increase in the volume of medial dendrites under the action of L-dopa, then beta-amyloid. Pathological changes in the ultrastructure of neurons and afferent synapses were not found, but signs of early amyloidosis were revealed.Conclusions. The use of L-dopa slows down the degeneration of Mauthner's neurons. It has been suggested that the resistance of whole neurons to the neurotoxic action of beta-amyloid is due to the mechanism of structural homeostasis aimed at compensatory restoration of the morphological organization of neurons.","PeriodicalId":74228,"journal":{"name":"Morphology (Dordrecht, Netherlands)","volume":"172 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2022-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"The use of L-dopa induces the resistance of Mauthner's neurons to the neurotoxic action of beta-amyloid\",\"authors\":\"N. R. Tiras, I. Mikheeva, Gulnara Mihailova, N. Penkova, Sergey Surenovich Khutzian\",\"doi\":\"10.17816/morph.89904\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Objective - to study the three-dimensional structure of Mauthner neurons in goldfish and the ultrastructure of their afferent synapses under the influence of L-dopa and the toxic fragment of 25-35 beta-amyloid.Materials and methods. The study was performed on Mauthner neurons of the goldfish fry (n=12) by the methods of light and electron microscopy. The identification of Mauthner's neurons and the reconstruction of their integral structure, the determination of the volume of the soma, ventral and lateral dendrites and the study of the structure of afferent synapses were carried out using serial sections 3 m thick.Results. The use of L-dopa stabilizes the size of the soma and ventral dendrites. A decrease in the volume of the lateral dendrite is accompanied either by an increase in the volume of its branches under the action of beta-amyloid, then L-dopa, or an increase in the volume of medial dendrites under the action of L-dopa, then beta-amyloid. Pathological changes in the ultrastructure of neurons and afferent synapses were not found, but signs of early amyloidosis were revealed.Conclusions. The use of L-dopa slows down the degeneration of Mauthner's neurons. It has been suggested that the resistance of whole neurons to the neurotoxic action of beta-amyloid is due to the mechanism of structural homeostasis aimed at compensatory restoration of the morphological organization of neurons.\",\"PeriodicalId\":74228,\"journal\":{\"name\":\"Morphology (Dordrecht, Netherlands)\",\"volume\":\"172 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2022-12-17\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Morphology (Dordrecht, Netherlands)\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.17816/morph.89904\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Morphology (Dordrecht, Netherlands)","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17816/morph.89904","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
The use of L-dopa induces the resistance of Mauthner's neurons to the neurotoxic action of beta-amyloid
Objective - to study the three-dimensional structure of Mauthner neurons in goldfish and the ultrastructure of their afferent synapses under the influence of L-dopa and the toxic fragment of 25-35 beta-amyloid.Materials and methods. The study was performed on Mauthner neurons of the goldfish fry (n=12) by the methods of light and electron microscopy. The identification of Mauthner's neurons and the reconstruction of their integral structure, the determination of the volume of the soma, ventral and lateral dendrites and the study of the structure of afferent synapses were carried out using serial sections 3 m thick.Results. The use of L-dopa stabilizes the size of the soma and ventral dendrites. A decrease in the volume of the lateral dendrite is accompanied either by an increase in the volume of its branches under the action of beta-amyloid, then L-dopa, or an increase in the volume of medial dendrites under the action of L-dopa, then beta-amyloid. Pathological changes in the ultrastructure of neurons and afferent synapses were not found, but signs of early amyloidosis were revealed.Conclusions. The use of L-dopa slows down the degeneration of Mauthner's neurons. It has been suggested that the resistance of whole neurons to the neurotoxic action of beta-amyloid is due to the mechanism of structural homeostasis aimed at compensatory restoration of the morphological organization of neurons.