Compensatory Changes in Mauthner Neurons in Goldfish Induced by Sensory Stimulation and Application of β-Amyloid
Objectives. To study the structure and formation of Mauthner neuron dendrites in goldfish exposed to neurotoxic β-amyloid fragment 25–35 and prolonged sensory stimulation influencing the afferent inputs to these neurons. Materials and methods. Goldfish Mauthner neurons were studied by light and elec...
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Veröffentlicht in: | Neuroscience and behavioral physiology 2019-07, Vol.49 (6), p.784-790 |
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creator | Tiras, N. R. Mikheyeva, I. B. Mikhailova, G. Z. Pen’kova, N. A. Bezgina, Ye. N. |
description | Objectives.
To study the structure and formation of Mauthner neuron dendrites in goldfish exposed to neurotoxic β-amyloid fragment 25–35 and prolonged sensory stimulation influencing the afferent inputs to these neurons.
Materials and methods.
Goldfish Mauthner neurons were studied by light and electron microscopy. Individual dendrites were identified, their volumes were determined, and synapse structure was assessed using virtual 3D images of Mauthner neurons obtained from serial sections of thickness 3 μm. The functional status of Mauthner neurons was evaluated indirectly from the motor lateralization of the fish.
Results.
Mauthner neurons responded to application of β-amyloid combined with subsequent prolonged sensory stimulation with decreases in the volume of the ventral dendrites, damage to their ultrastructure, and degeneration of a proportion of synapses. Degeneration of more active neurons was more significant than that of less active cells. Newly formed medial dendrites had greater volume and less damaged synapse ultrastructure than ventral dendrites. There were no differences in the sizes of specialized junctions between synapses of the same type on ventral and medial synapses.
Conclusions.
Medial dendrite formation is a compensatory reaction to dystrophy of the ventral dendrite due to the experimental treatment. |
doi_str_mv | 10.1007/s11055-019-00802-3 |
format | Article |
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To study the structure and formation of Mauthner neuron dendrites in goldfish exposed to neurotoxic β-amyloid fragment 25–35 and prolonged sensory stimulation influencing the afferent inputs to these neurons.
Materials and methods.
Goldfish Mauthner neurons were studied by light and electron microscopy. Individual dendrites were identified, their volumes were determined, and synapse structure was assessed using virtual 3D images of Mauthner neurons obtained from serial sections of thickness 3 μm. The functional status of Mauthner neurons was evaluated indirectly from the motor lateralization of the fish.
Results.
Mauthner neurons responded to application of β-amyloid combined with subsequent prolonged sensory stimulation with decreases in the volume of the ventral dendrites, damage to their ultrastructure, and degeneration of a proportion of synapses. Degeneration of more active neurons was more significant than that of less active cells. Newly formed medial dendrites had greater volume and less damaged synapse ultrastructure than ventral dendrites. There were no differences in the sizes of specialized junctions between synapses of the same type on ventral and medial synapses.
Conclusions.
Medial dendrite formation is a compensatory reaction to dystrophy of the ventral dendrite due to the experimental treatment.</description><identifier>ISSN: 0097-0549</identifier><identifier>EISSN: 1573-899X</identifier><identifier>DOI: 10.1007/s11055-019-00802-3</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Alzheimer's disease ; Behavioral Sciences ; Biomedical and Life Sciences ; Biomedicine ; Degeneration ; Dendrites ; Dystrophy ; Electron microscopy ; Neurobiology ; Neurons ; Neurosciences ; Neurotoxicity ; Sensory neurons ; Sensory stimulation ; Synapses ; Synaptogenesis ; Ultrastructure ; β-Amyloid</subject><ispartof>Neuroscience and behavioral physiology, 2019-07, Vol.49 (6), p.784-790</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Neuroscience and Behavioral Physiology is a copyright of Springer, (2019). All Rights Reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c2343-270c22d9588487067390bb52cfd073ab232a15e7cd55c45ec1ab999d5e63a1873</citedby><cites>FETCH-LOGICAL-c2343-270c22d9588487067390bb52cfd073ab232a15e7cd55c45ec1ab999d5e63a1873</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s11055-019-00802-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s11055-019-00802-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids></links><search><creatorcontrib>Tiras, N. R.</creatorcontrib><creatorcontrib>Mikheyeva, I. B.</creatorcontrib><creatorcontrib>Mikhailova, G. Z.</creatorcontrib><creatorcontrib>Pen’kova, N. A.</creatorcontrib><creatorcontrib>Bezgina, Ye. N.</creatorcontrib><title>Compensatory Changes in Mauthner Neurons in Goldfish Induced by Sensory Stimulation and Application of β-Amyloid</title><title>Neuroscience and behavioral physiology</title><addtitle>Neurosci Behav Physi</addtitle><description>Objectives.
To study the structure and formation of Mauthner neuron dendrites in goldfish exposed to neurotoxic β-amyloid fragment 25–35 and prolonged sensory stimulation influencing the afferent inputs to these neurons.
Materials and methods.
Goldfish Mauthner neurons were studied by light and electron microscopy. Individual dendrites were identified, their volumes were determined, and synapse structure was assessed using virtual 3D images of Mauthner neurons obtained from serial sections of thickness 3 μm. The functional status of Mauthner neurons was evaluated indirectly from the motor lateralization of the fish.
Results.
Mauthner neurons responded to application of β-amyloid combined with subsequent prolonged sensory stimulation with decreases in the volume of the ventral dendrites, damage to their ultrastructure, and degeneration of a proportion of synapses. Degeneration of more active neurons was more significant than that of less active cells. Newly formed medial dendrites had greater volume and less damaged synapse ultrastructure than ventral dendrites. There were no differences in the sizes of specialized junctions between synapses of the same type on ventral and medial synapses.
Conclusions.
Medial dendrite formation is a compensatory reaction to dystrophy of the ventral dendrite due to the experimental treatment.</description><subject>Alzheimer's disease</subject><subject>Behavioral Sciences</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Degeneration</subject><subject>Dendrites</subject><subject>Dystrophy</subject><subject>Electron microscopy</subject><subject>Neurobiology</subject><subject>Neurons</subject><subject>Neurosciences</subject><subject>Neurotoxicity</subject><subject>Sensory neurons</subject><subject>Sensory stimulation</subject><subject>Synapses</subject><subject>Synaptogenesis</subject><subject>Ultrastructure</subject><subject>β-Amyloid</subject><issn>0097-0549</issn><issn>1573-899X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNp9kM1KAzEURoMoWKsv4CrgOnqTNGayLMWfQtWFCu5CJsnYKdNkmsws-lo-iM_k6AjuXF3u5TvfhYPQOYVLCiCvMqUgBAGqCEABjPADNKFCclIo9XaIJgBKEhAzdYxOct7AAMkCJmi3iNvWh2y6mPZ4sTbh3WdcB_xg-m4dfMKPvk8x_NzuYuOqOq_xMrjeeofLPX4e4G_0uau3fWO6OgZsgsPztm1qO-6xwp8fZL7dN7F2p-ioMk32Z79zil5vb14W92T1dLdczFfEMj7jhEmwjDklimJWSLiWXEFZCmYrB5KbknFmqPDSOiHsTHhLTamUcsJfc0MLyafoYuxtU9z1Pnd6E_sUhpeaMaEolYqLIcXGlE0x5-Qr3aZ6a9JeU9DfavWoVg9q9Y9azQeIj1AewoOw9Ff9D_UFYyF8_w</recordid><startdate>20190715</startdate><enddate>20190715</enddate><creator>Tiras, N. R.</creator><creator>Mikheyeva, I. B.</creator><creator>Mikhailova, G. Z.</creator><creator>Pen’kova, N. A.</creator><creator>Bezgina, Ye. 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B. ; Mikhailova, G. Z. ; Pen’kova, N. A. ; Bezgina, Ye. N.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c2343-270c22d9588487067390bb52cfd073ab232a15e7cd55c45ec1ab999d5e63a1873</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Alzheimer's disease</topic><topic>Behavioral Sciences</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Degeneration</topic><topic>Dendrites</topic><topic>Dystrophy</topic><topic>Electron microscopy</topic><topic>Neurobiology</topic><topic>Neurons</topic><topic>Neurosciences</topic><topic>Neurotoxicity</topic><topic>Sensory neurons</topic><topic>Sensory stimulation</topic><topic>Synapses</topic><topic>Synaptogenesis</topic><topic>Ultrastructure</topic><topic>β-Amyloid</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Tiras, N. R.</creatorcontrib><creatorcontrib>Mikheyeva, I. B.</creatorcontrib><creatorcontrib>Mikhailova, G. Z.</creatorcontrib><creatorcontrib>Pen’kova, N. A.</creatorcontrib><creatorcontrib>Bezgina, Ye. N.</creatorcontrib><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><jtitle>Neuroscience and behavioral physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Tiras, N. R.</au><au>Mikheyeva, I. B.</au><au>Mikhailova, G. Z.</au><au>Pen’kova, N. A.</au><au>Bezgina, Ye. N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Compensatory Changes in Mauthner Neurons in Goldfish Induced by Sensory Stimulation and Application of β-Amyloid</atitle><jtitle>Neuroscience and behavioral physiology</jtitle><stitle>Neurosci Behav Physi</stitle><date>2019-07-15</date><risdate>2019</risdate><volume>49</volume><issue>6</issue><spage>784</spage><epage>790</epage><pages>784-790</pages><issn>0097-0549</issn><eissn>1573-899X</eissn><abstract>Objectives.
To study the structure and formation of Mauthner neuron dendrites in goldfish exposed to neurotoxic β-amyloid fragment 25–35 and prolonged sensory stimulation influencing the afferent inputs to these neurons.
Materials and methods.
Goldfish Mauthner neurons were studied by light and electron microscopy. Individual dendrites were identified, their volumes were determined, and synapse structure was assessed using virtual 3D images of Mauthner neurons obtained from serial sections of thickness 3 μm. The functional status of Mauthner neurons was evaluated indirectly from the motor lateralization of the fish.
Results.
Mauthner neurons responded to application of β-amyloid combined with subsequent prolonged sensory stimulation with decreases in the volume of the ventral dendrites, damage to their ultrastructure, and degeneration of a proportion of synapses. Degeneration of more active neurons was more significant than that of less active cells. Newly formed medial dendrites had greater volume and less damaged synapse ultrastructure than ventral dendrites. There were no differences in the sizes of specialized junctions between synapses of the same type on ventral and medial synapses.
Conclusions.
Medial dendrite formation is a compensatory reaction to dystrophy of the ventral dendrite due to the experimental treatment.</abstract><cop>New York</cop><pub>Springer US</pub><doi>10.1007/s11055-019-00802-3</doi><tpages>7</tpages></addata></record> |
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subjects | Alzheimer's disease Behavioral Sciences Biomedical and Life Sciences Biomedicine Degeneration Dendrites Dystrophy Electron microscopy Neurobiology Neurons Neurosciences Neurotoxicity Sensory neurons Sensory stimulation Synapses Synaptogenesis Ultrastructure β-Amyloid |
title | Compensatory Changes in Mauthner Neurons in Goldfish Induced by Sensory Stimulation and Application of β-Amyloid |
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