Syncytial coupling of neurons in tissue culture and early ontogenesis

Os, Sotnikov; Малашко, В В; Rybakova, G. I.

doi:10.1007/s11055-008-0045-8

Cited by 7 publications

(6 citation statements)

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“…Perforations and fusions of filopodia have been shown in growth cones (Spooner et al, 1974). Syncytial connections between axons and dendrites have been found in large cerebral hemispheres in normal conditions (Santander et al, 1988) and in pathology (Samosudova et al, 2007) as well as in the intramural autonomic nervous system (Sotnikov et al, 2006, 2008). Earlier, the syncytial connection and fusion of nerve processes were identified in giant axons of cephalopod molluscs, crustaceans and polychaetes (Young, 1938; Nicol, 1948).…”

Section: Introductionmentioning

confidence: 99%

Ultrastructural analysis of interneuronal syncytial perforations

Paramonova

Арчакова

2010

Cell Biology International

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The structural regularities of the organization of interneuronal syncytial cytoplasmic connections between neuronal bodies in gyrus dentatus and CA1 and CA2 (CA is cornu ammonis) of hippocampus, as well as between cell neurites of the caudal mesenteric ganglion were studied by transmission electron microscopy. The syncytial perforations are located only on the base of tight junctions. The perforations have rounded edges corresponding to the fusion edges of perforated membranes of adjacent neurons - or where their edges have a form of thinned plate - a remnant of the tight junction. In the lumen of the perforations, remnants of contact membranes - residual bodies - are revealed. On living neurons in tissue culture, the syncytial connection of two contacting processes of different neurons is found during the death of the body of one of them, but with preservation of viability of its processes that contact with other neurons.

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Section: Introductionmentioning

confidence: 99%

Ultrastructural analysis of interneuronal syncytial perforations

Paramonova

Арчакова

2010

Cell Biology International

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“…В лаборатории профессора О.С. Сотникова на протяжении многих лет подробно изучали механизм слияния нейронов посредством образования синцитиальной связи, приводящий к появлению многоядерных клеток [56]. Не исключено, что подобные слияния нейронов происходят с целью осуществления репаративных процессов при возникновении неблагоприятных условий.…”

Section: анеуплоидия и полиплоидия в головном мозге при старении и боunclassified

Morphofunctional Changes and Compensatory Mechanisms in the Human Brain with Aging and in Alzheimer's Disease

Ishunina

Bogolepova

Swaab

2020

Žurnal anatomii i gistopatologii

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The article focuses on age-related morphofunctional changes in the human brain and the issue of compensatory-adaptive mechanisms developed in normal aging. According to the scientific literature, the volume of white matter is reduced to a greater extent with aging, the fact associating with myelin fibers degeneration, the appearance of Virchow–Robin spaces and a decrease in the effectiveness of the blood-brain barrier. Atrophic processes in gray matter are currently associated not only with the death of neurons, but with degenerative changes in synapses, a decrease in their number, and reduction of dendritic branches and spines. A decrease in the size of pericarions resulting in a decrease in the number of large neurocytes and an increase in the proportion of small neurons is noted in certain brain structures. However, age-related neuronal hypertrophy is observed in the nuclei of the hypothalamus, Meinert’s basal nucleus. This is mostly manifested in the female group, and is undoubtedly associated with a decrease in estrogen levels and the period of menopause. An increase in the metabolic activity of neurons manifested by related changes in the size of the pericarions and nuclei of neurons and their Golgi complex can be attributed to compensatory-adaptive mechanisms that can delay or prevent the development of neurodegenerative disorders, such as Alzheimer's disease. Neurons with a higher metabolic activity have better ability to self-repair. Due to this, neuron reactivation techniques are being developed with aging based on the selection of the correct stimulus. The growth of the glial cell population is also considered to be compensatory, since these cells are crucial for neuron adaptation and able to affect the level of neuronal RNA synthesis. Furthermore, the article highlights literature data on possible triggers of the compensatory capabilities of the brain with aging and under pathological processes.

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“…For example, the giant axons of the squid are generated by complete fusion of multiple neurons (third order giant fibers) and the syncytial axon is enclosed in a single sheath cell 27 . In vertebrates, some studies using electron microscopy and brightfield microscopy have reported the formation of neuronal syncytia in vitro and in vivo [28][29][30][31][32] ; unfortunately, however, these results were not quantified, making it difficult to determine their general relevance. Overall, the vast majority of neuronal cell-cell fusion events in different species have been described in the context of specific conditions or insults, which include viral infection, axonal injury, or the presence of stem or precursor cells ( Figure 5.2 and Table 5.1).…”

Section: Neuronal Cell-cell Fusion and Its Implicationsmentioning

confidence: 99%

“…Recruitment of EFF-1 to fusion sites in larval hypodermal cells was shown to be mediated at least in part by the actin regulator ), but other pathways may also exist. Much has been characterized about the molecular cascades that are activated in regenerating axons [28][29][30] and it is plausible that some of these molecules play a currently uncharacterized role in EFF-1 recruitment. …”

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confidence: 99%

“…This molecule is also able to mediate membrane fusion in vitro in other cellular contexts [26][27][28][29][30][31] . EFF-1 must be inserted into both membranes to mediate fusion; current models suggest that its mechanism of action involves the formation of trimers in trans across apposing membranes 28,31 . Its activity is known to be precisely regulated in development, ensuring it mediates fusion at the correct place and time 23, .…”

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confidence: 99%

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Function and regulation of the fusogen EFF-1 during axonal repair

Linton¹

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In the current clinical environment, treatment options for nerve and spinal cord injuries remain limited. To develop novel therapies, we require a better understanding of axonal repair and its underlying molecular mechanisms. The response of an axon to a transection injury is complex: the axon still attached to the cell body begins a process of regenerative regrowth, whereas a concurrent process of degeneration is activated in the severed axonal fragment. Characterizing ways in which the axon can achieve repair, involving both regeneration and degeneration, is crucial to making progress in a clinical setting.We have studied a means of axonal repair called axonal fusion, which occurs spontaneously in the mechanosensory neurons of the nematode C. elegans. Following axotomy with a UV laser, the regrowing axonal fragment is able to directly fuse with its own severed fragment, re-establishing continuity. When axonal fusion was first described in C. elegans, the molecular pathways involved were unknown, and the only protein associated with the process was the fusogen Epithelial Fusion Failure-1 (EFF-1). EFF-1 is a nematode-specific transmembrane glycoprotein that acts to fuse plasma membranes. It has been studied extensively in other C. elegans tissues, but its function and regulation in neurons have been largely uncharacterized.In this context, we aimed to further understand the role of EFF-1 in axonal repair, focusing on its potential contribution to both regeneration and degeneration, and the mechanisms that regulate its fusogenic activity. We approached these biological questions using a combination of genetic and molecular biology techniques available in the C. elegans model system.The following chapters characterize EFF-1 function and regulation in the C. elegans mechanosensory neuron PLM. Firstly, we demonstrate a cell-autonomous role for EFF-1 in axonal fusion, and show that it has a dynamic localization pattern in the regenerating axon, whereby it is mobilized to the membrane of the regenerating growth cone. We also place it downstream in a pathway of apoptotic clearance molecules that allow recognition of the distal axonal fragment.Secondly, we find that neuronal EFF-1 is regulated by the endocytic GTPase RAB-5, with alterations in RAB-5 activity affecting both EFF-1 localization and its function in axonal fusion.Thirdly, we characterize the genes involved in the degeneration of the distal PLM axon following axotomy, and find a remarkable overlap with the molecules involved in regenerative fusion, possibly including EFF-1. Finally, we discuss an intriguing potential role for EFF-1 in mediating neuronal repair through cell-cell fusion. The research detailed here represents significant progress in understanding how a fusogen mediates axonal repair in vivo. It will potentially contribute to the application of axonal fusion as a novel therapy for patients with nerve injuries.ii Declaration by authorThis thesis is composed of my original work, and contains no material previously published or written by an...

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Syncytial coupling of neurons in tissue culture and early ontogenesis

Cited by 7 publications

References 41 publications

Ultrastructural analysis of interneuronal syncytial perforations

Ultrastructural analysis of interneuronal syncytial perforations

Morphofunctional Changes and Compensatory Mechanisms in the Human Brain with Aging and in Alzheimer's Disease

Function and regulation of the fusogen EFF-1 during axonal repair

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