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Li-ru Zhao - One of the best experts on this subject based on the ideXlab platform.
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SCF + G-CSF treatment in the chronic phase of severe TBI enhances axonal sprouting in the spinal cord and Synaptic Pruning in the hippocampus.
Acta neuropathologica communications, 2021Co-Authors: Xuecheng Qiu, Suning Ping, Michele Kyle, Lawrence Chin, Li-ru ZhaoAbstract:Traumatic brain injury (TBI) is a major cause of long-term disability in young adults. An evidence-based treatment for TBI recovery, especially in the chronic phase, is not yet available. Using a severe TBI mouse model, we demonstrate that the neurorestorative efficacy of repeated treatments with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) (SCF + G-CSF) in the chronic phase is superior to SCF + G-CSF single treatment. SCF + G-CSF treatment initiated at 3 months post-TBI enhances contralesional corticospinal tract sprouting into the denervated side of the cervical spinal cord and re-balances the TBI-induced overgrown synapses in the hippocampus by enhancing microglial function of Synaptic Pruning. These neurorestorative changes are associated with SCF + G-CSF-improved somatosensory-motor function and spatial learning. In the chronic phase of TBI, severe TBI-caused microglial degeneration in the cortex and hippocampus is ameliorated by SCF + G-CSF treatment. These findings reveal the therapeutic potential and possible mechanism of SCF + G-CSF treatment in brain repair during the chronic phase of severe TBI.
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scf g csf treatment in the chronic phase of severe tbi enhances axonal sprouting in the spinal cord and Synaptic Pruning in the hippocampus
Acta neuropathologica communications, 2021Co-Authors: Xuecheng Qiu, Suning Ping, Michele Kyle, Lawrence S Chin, Li-ru ZhaoAbstract:Traumatic brain injury (TBI) is a major cause of long-term disability in young adults. An evidence-based treatment for TBI recovery, especially in the chronic phase, is not yet available. Using a severe TBI mouse model, we demonstrate that the neurorestorative efficacy of repeated treatments with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) (SCF + G-CSF) in the chronic phase is superior to SCF + G-CSF single treatment. SCF + G-CSF treatment initiated at 3 months post-TBI enhances contralesional corticospinal tract sprouting into the denervated side of the cervical spinal cord and re-balances the TBI-induced overgrown synapses in the hippocampus by enhancing microglial function of Synaptic Pruning. These neurorestorative changes are associated with SCF + G-CSF-improved somatosensory-motor function and spatial learning. In the chronic phase of TBI, severe TBI-caused microglial degeneration in the cortex and hippocampus is ameliorated by SCF + G-CSF treatment. These findings reveal the therapeutic potential and possible mechanism of SCF + G-CSF treatment in brain repair during the chronic phase of severe TBI.
Li-jen Lee - One of the best experts on this subject based on the ideXlab platform.
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0285 Preventative Voluntary Exercise Ameliorate Synaptic-Pruning Defects on Sleep-Deprived Adolescent
Sleep, 2020Co-Authors: L Tuan, C Tsao, Li-jen LeeAbstract:Abstract Introduction Since adolescent is a critical period for brain development, adequate sleep during this period is essential to cognitive performance as well as the psychological health in later life. Emerging evidence on sleep-deprived animal models has detailed the impacts of sleep loss on the developing brain. For instance, our previous study demonstrated that 72 h sleep deprivation (SD) disrupted microglia-mediated Synaptic refinement in the dentate gyrus (DG). Physical exercise is proved to counteract the harmful consequences of various stress or neurodegenerative models by modulating microglial function. Therefore, we hypothesized that physical exercise might be a preventive intervention to rescue the failure of Synaptic Pruning and microglial function after SD in adolescent mice. Methods C57/BL6 male mice 3 weeks were assigned to the home cage (HC), home cage with voluntary exercise (HC+VE), sleep deprivation (SD), or sleep deprivation with voluntary exercise (SD+VE) group. In the groups with VE, a running wheel was placed in the cage 11 days before the SD paradigm. Following 72 h SD, animals were subjected to a short-term memory test or sacrificed directly for further examination. Results Our results showed that impaired memory performance was reversed in sleep-deprived mice after VE. Also, the SD+VE group exhibited less dendritic spine density compared to the SD group, implying VE rescue the Synaptic Pruning defect after SD. Greater microglia phagocytic ability, characterized by increased internalized postSynaptic materials and lysosomal structure within individual microglia, were observed in the SD+VE compared to the SD group. We also investigated the mRNA expression of microglia-specific receptors critical to developmental Synaptic refinement and found an upregulation of CX3CR1 expression in both HC+VE and SD+VE compared to sedentary groups. Conclusion Here we provided evidence featuring that developmental VE significantly alleviated the SD-induced memory defects. Moreover, the SD-induced Synaptic Pruning impairment and microglial maladaptation were also prevented by the VE regimen, suggesting that physical exercise is a possible therapeutic interventions to the cognitive performance as well as the developmental trajectories to the adolescent brain under the influence of sleep insufficiency. Support Supported by the Ministry of Science and Technology of the Republic of China (Grant number: 104-2314-B-002-129-MY4).
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Microglia-mediated Synaptic Pruning is impaired in sleep-deprived adolescent mice.
Neurobiology of Disease, 2019Co-Authors: Li-heng Tuan, Li-jen LeeAbstract:Abstract The detrimental effects of sleep insufficiency have been extensively explored. However, only a few studies have addressed this issue in adolescents. In the present study, we examined and compared the effects of 72 h paradoxical sleep deprivation (SD) on adolescent (5 weeks old) and adult (~12 weeks old) mice. Following 72 h of SD, induced by a modified multiple-platform method, mice were subjected to behavioral, histological and neurochemical examinations. In both adolescent and adult mice, SD adversely affected short-term memory in a novel object recognition test. Compared with normal-sleep controls, sleep-deprived adolescent mice had an increased density of excitatory synapses in the granule cells of the dentate gyrus, but no such pattern was observed in the adult group. The engulfment of postSynaptic components within the microglia after SD was reduced in adolescents but not in adults, suggesting an impaired microglia-mediated Synaptic Pruning in adolescent SD mice. Possible contributing factors included the decreases in CX3CR1, CD11b and P2Y12, closely associated with the Synaptic Pruning via microglial phagocytosis. In adult SD mice, microglia-associated inflammatory reactions were noted. In sum, sleep deprivation induces age-dependent microglial reactions in adolescent and adult mice, respectively; yet results in similar defects in short-term recognition memory. Sufficient sleep is indispensable for adolescents and adults.
Xuecheng Qiu - One of the best experts on this subject based on the ideXlab platform.
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SCF + G-CSF treatment in the chronic phase of severe TBI enhances axonal sprouting in the spinal cord and Synaptic Pruning in the hippocampus.
Acta neuropathologica communications, 2021Co-Authors: Xuecheng Qiu, Suning Ping, Michele Kyle, Lawrence Chin, Li-ru ZhaoAbstract:Traumatic brain injury (TBI) is a major cause of long-term disability in young adults. An evidence-based treatment for TBI recovery, especially in the chronic phase, is not yet available. Using a severe TBI mouse model, we demonstrate that the neurorestorative efficacy of repeated treatments with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) (SCF + G-CSF) in the chronic phase is superior to SCF + G-CSF single treatment. SCF + G-CSF treatment initiated at 3 months post-TBI enhances contralesional corticospinal tract sprouting into the denervated side of the cervical spinal cord and re-balances the TBI-induced overgrown synapses in the hippocampus by enhancing microglial function of Synaptic Pruning. These neurorestorative changes are associated with SCF + G-CSF-improved somatosensory-motor function and spatial learning. In the chronic phase of TBI, severe TBI-caused microglial degeneration in the cortex and hippocampus is ameliorated by SCF + G-CSF treatment. These findings reveal the therapeutic potential and possible mechanism of SCF + G-CSF treatment in brain repair during the chronic phase of severe TBI.
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scf g csf treatment in the chronic phase of severe tbi enhances axonal sprouting in the spinal cord and Synaptic Pruning in the hippocampus
Acta neuropathologica communications, 2021Co-Authors: Xuecheng Qiu, Suning Ping, Michele Kyle, Lawrence S Chin, Li-ru ZhaoAbstract:Traumatic brain injury (TBI) is a major cause of long-term disability in young adults. An evidence-based treatment for TBI recovery, especially in the chronic phase, is not yet available. Using a severe TBI mouse model, we demonstrate that the neurorestorative efficacy of repeated treatments with stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) (SCF + G-CSF) in the chronic phase is superior to SCF + G-CSF single treatment. SCF + G-CSF treatment initiated at 3 months post-TBI enhances contralesional corticospinal tract sprouting into the denervated side of the cervical spinal cord and re-balances the TBI-induced overgrown synapses in the hippocampus by enhancing microglial function of Synaptic Pruning. These neurorestorative changes are associated with SCF + G-CSF-improved somatosensory-motor function and spatial learning. In the chronic phase of TBI, severe TBI-caused microglial degeneration in the cortex and hippocampus is ameliorated by SCF + G-CSF treatment. These findings reveal the therapeutic potential and possible mechanism of SCF + G-CSF treatment in brain repair during the chronic phase of severe TBI.
Alessandro E P Villa - One of the best experts on this subject based on the ideXlab platform.
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stimulus driven unsupervised Synaptic Pruning in large neural networks
Lecture Notes in Computer Science, 2005Co-Authors: Javier Iglesias, Jan Eriksson, Beatriz Pardo, Marco Tomassini, Alessandro E P VillaAbstract:We studied the emergence of cell assemblies out of locally connected random networks of integrate-and-fire units distributed on a 2D lattice stimulated with a spatiotemporal pattern in presence of independent random background noise. Networks were composed of 80% excitatory and 20% inhibitory units with initially balanced Synaptic weights. Excitatory–excitatory synapses were modified according to a spike-timing-dependent Synaptic plasticity (stdp) rule associated with Synaptic Pruning. We show that the application, in presence of background noise, of a recurrent pattern of stimulation let appear cell assemblies characterized by an internal pattern of converging projections and a feed-forward topology not observed with an equivalent random stimulation.
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BVAI - Stimulus-driven unsupervised Synaptic Pruning in large neural networks
Brain Vision and Artificial Intelligence, 2005Co-Authors: Javier Iglesias, Jan Eriksson, Beatriz Pardo, Marco Tomassini, Alessandro E P VillaAbstract:We studied the emergence of cell assemblies out of locally connected random networks of integrate-and-fire units distributed on a 2D lattice stimulated with a spatiotemporal pattern in presence of independent random background noise. Networks were composed of 80% excitatory and 20% inhibitory units with initially balanced Synaptic weights. Excitatory–excitatory synapses were modified according to a spike-timing-dependent Synaptic plasticity (stdp) rule associated with Synaptic Pruning. We show that the application, in presence of background noise, of a recurrent pattern of stimulation let appear cell assemblies characterized by an internal pattern of converging projections and a feed-forward topology not observed with an equivalent random stimulation.
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Dynamics of Pruning in simulated large-scale spiking neural networks.
Biosystems, 2005Co-Authors: Javier Iglesias, Jan Eriksson, Marco Tomassini, François Grize, Alessandro E P VillaAbstract:Massive Synaptic Pruning following over-growth is a general feature of mammalian brain maturation. This article studies the Synaptic Pruning that occurs in large networks of simulated spiking neurons in the absence of specific input patterns of activity. The evolution of connections between neurons were governed by an original bioinspired spike-timing-dependent Synaptic plasticity (STDP) modification rule which included a slow decay term. The network reached a steady state with a bimodal distribution of the Synaptic weights that were either incremented to the maximum value or decremented to the lowest value. After 1x10(6) time steps the final number of synapses that remained active was below 10% of the number of initially active synapses independently of network size. The Synaptic modification rule did not introduce spurious biases in the geometrical distribution of the remaining active projections. The results show that, under certain conditions, the model is capable of generating spontaneously emergent cell assemblies.
Thomas H. Mcglashan - One of the best experts on this subject based on the ideXlab platform.
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NMDA-receptor hypofunction versus excessive Synaptic elimination as models of schizophrenia
Behavioral and Brain Sciences, 2003Co-Authors: Ralph E. Hoffman, Thomas H. McglashanAbstract:AbstractWe propose that the primary cause of schizophrenia is a pathological extension of Synaptic Pruning involving local connectivity that unfolds ordinarily during adolescence. Computer simulations suggest that this pathology provides reasonable accounts of a range of symptoms in schizophrenia, and is consistent with recent postmortem and genetic studies. NMDA-receptors play a regulatory role in maintaining and/or eliminating cortical synapses, and therefore may play a pathophysiological role.
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N-Methyl-D-Aspartate Receptor Hypofunction in Schizophrenia Could Arise From Reduced Cortical Connectivity Rather Than Receptor Dysfunction
Archives of General Psychiatry, 1997Co-Authors: Ralph E. Hoffman, Thomas H. McglashanAbstract:Hoffman and McGlashan are generally accepting of our NMDA receptor hypofunction (NRH) hypothesis of schizophrenia, but they argue that NRH could arise from reduced cortical connectivity rather than receptor dysfunction per se, and in their closing paragraphs they introduce a neurodevelopmental twist (faulty Synaptic Pruning) that they would like to see emphasized in an alternate framing of our hypothesis. Implicit in their letter is the suggestion that reduced cortical connectivity, faulty Synaptic Pruning, and a neu
