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
Hauptverfasser: Tiras, N. R., Mikheyeva, I. B., Mikhailova, G. Z., Pen’kova, N. A., Bezgina, Ye. N.
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container_end_page 790
container_issue 6
container_start_page 784
container_title Neuroscience and behavioral physiology
container_volume 49
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
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R. ; Mikheyeva, I. B. ; Mikhailova, G. Z. ; Pen’kova, N. A. ; Bezgina, Ye. N.</creator><creatorcontrib>Tiras, N. R. ; Mikheyeva, I. B. ; Mikhailova, G. Z. ; Pen’kova, N. A. ; Bezgina, Ye. N.</creatorcontrib><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><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). 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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. 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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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