https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45247 Wed 26 Oct 2022 20:03:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33580 Wed 21 Nov 2018 16:34:27 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33581 Wed 21 Nov 2018 16:34:26 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33579 Wed 19 Jan 2022 15:18:17 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:23930 Wed 17 Nov 2021 16:31:15 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33577 in vitro and that C3a receptor signalling stimulates neurogenesis in unchallenged adult mice. To determine the role of C3a-C3a receptor signalling in ischaemia-induced neural plasticity, we subjected C3a receptor-deficient mice, GFAP-C3a transgenic mice expressing biologically active C3a in the central nervous system, and their respective wild-type controls to photothrombotic stroke. We found that C3a overexpression increased, whereas C3a receptor deficiency decreased post-stroke expression of GAP43 (P < 0.01), a marker of axonal sprouting and plasticity, in the peri-infarct cortex. To verify the translational potential of these findings, we used a pharmacological approach. Daily intranasal treatment of wild-type mice with C3a beginning 7 days after stroke induction robustly increased synaptic density (P < 0.01) and expression of GAP43 in peri-infarct cortex (P < 0.05). Importantly, the C3a treatment led to faster and more complete recovery of forepaw motor function (P < 0.05). We conclude that C3a-C3a receptor signalling stimulates post-ischaemic neural plasticity and intranasal treatment with C3a receptor agonists is an attractive approach to improve functional recovery after ischaemic brain injury.]]> Wed 17 Nov 2021 16:30:36 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50144 Wed 13 Mar 2024 08:54:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:15202 Wed 11 Apr 2018 15:20:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:14413 Wed 11 Apr 2018 14:45:30 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:30287 Wed 11 Apr 2018 12:31:05 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27925 Wed 10 Nov 2021 15:05:24 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50139 Wed 05 Jul 2023 12:54:49 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33578 Wed 04 Sep 2019 09:48:09 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49081 Wed 03 May 2023 16:22:13 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48116 Wed 01 Mar 2023 13:27:10 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44249 GFAP^-/-Vim^-/-) exhibit increased post-traumatic synaptic plasticity and increased basal and post-traumatic hippocampal neurogenesis. Here we assessed the locomotor and exploratory behavior of GFAP^-/-Vim^-/- mice, their learning, memory and memory extinction, by using the open field, object recognition and Morris water maze tests, trace fear conditioning, and by recording reversal learning in IntelliCages. While the locomotion, exploratory behavior and learning of GFAP^-/-Vim^-/- mice, as assessed by object recognition, the Morris water maze, and trace fear conditioning tests, were comparable to wildtype mice, GFAP^-/-Vim^-/- mice showed more pronounced memory extinction when tested in IntelliCages, a finding compatible with the scenario of an increased rate of reorganization of the hippocampal circuitry.]]> Tue 11 Oct 2022 12:10:20 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33582 SA/SA) leads to cytokinetic failures in fibroblasts and lens epithelial cells, resulting in chromosomal instability and increased expression of cell senescence markers. In this study, we investigated morphology, proliferative capacity, and motility of VIM^SA/SA astrocytes, and their effect on the differentiation of neural stem/progenitor cells. VIM^SA/SA astrocytes expressed less vimentin and more GFAP but showed a well-developed intermediate filament network, exhibited normal cell morphology, proliferation, and motility in an in vitro wound closing assay. Interestingly, we found a two- to fourfold increased neuronal differentiation of VIM^SA/SA neurosphere cells, both in a standard 2D and in Bioactive3D cell culture systems, and determined that this effect was neurosphere cell autonomous and not dependent on cocultured astrocytes. Using BrdU in vivo labeling to assess neural stem/progenitor cell proliferation and differentiation in the hippocampus of adult mice, one of the two major adult neurogenic regions, we found a modest increase (by 8%) in the fraction of newly born and surviving neurons. Thus, mutation of the serine sites phosphorylated in vimentin during mitosis alters intermediate filament protein expression but has no effect on astrocyte morphology or proliferation, and leads to increased neuronal differentiation of neural progenitor cells.]]> Tue 03 Sep 2019 17:59:31 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41004 Thu 21 Jul 2022 10:51:14 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:19423 −/− Vim ^−/−) do not form cytoplasmic intermediate filaments. GFAP ^−/− Vim ^−/− mice develop larger infarcts after ischemic stroke (Li et al. in J Cereb Blood Flow Metab 28(3):468–481, 2008). Here, we attempted to analyze the underlying mechanisms using oxygen–glucose deprivation (OGD), an in vitro ischemia model, examining a potential link between astrocyte intermediate filaments and reactive oxygen species (ROS). We observed a reorganization of the intermediate filament network in astrocytes exposed to OGD. ROS accumulation was higher in GFAP ^−/− Vim ^−/− than wild-type astrocytes when exposed to OGD followed by reperfusion or when exposed to hydrogen peroxide. These results indicate that the elimination of ROS is impaired in the absence of the intermediate filament system. Compared to wild-type astrocytes, GFAP ^−/− Vim ^−/− astrocytes exposed to OGD and reperfusion exhibited increased cell death and conferred lower degree of protection to cocultured neurons. We conclude that the astrocyte intermediate filament system is important for the cell response to oxidative stress induced by OGD followed by reperfusion.]]> Sat 24 Mar 2018 07:51:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27924 Sat 24 Mar 2018 07:36:08 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27422 POS or Aldh1L1^POS astrocytes freshly isolated from uninjured, contralesional and lesioned hippocampus 4 days after entorhinal cortex lesion. To determine the Notch signaling competence of individual astrocytes, we measured the mRNA levels of Notch ligands and Notch1 receptor. We found that whereas most cultured and freshly isolated astrocytes were competent to receive Notch signals, only a minority of astrocytes were competent to send Notch signals. Injury increased the fraction of astrocyte subpopulation unable to send and receive Notch signals, thus resembling primary astrocytes in vitro. Astrocytes deficient of GFAP and vimentin showed decreased Notch signal sending competence and altered expression of Notch signaling pathway-related genes Dlk2, Notch1, and Sox2. Furthermore, we identified astrocyte subpopulations based on their mRNA and protein expression of nestin and HB-EGF. This study improves our understanding of astrocyte heterogeneity, and points to astrocyte cytoplasmic intermediate filaments as targets for neural cell replacement strategies.]]> Sat 24 Mar 2018 07:35:23 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:27907 Sat 24 Mar 2018 07:24:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52857 Mon 30 Oct 2023 10:00:44 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:39237 -/-) mice were reported to exhibit subtle deficit in recall memory. Here, we subjected 3 months old male C3aR^-/- mice to a battery of behavioral tests and examined their brain morphology. We found that the C3aR^-/- mice exhibit a short-term memory deficit and increased locomotor activity, but do not show any signs of autistic behavior as assessed by self-grooming behavior. We also found regional differences between the C3aR^-/- and wild-type (WT) mice in the morphology of motor and somatosensory cortex, as well as amygdala and hippocampus. In summary, constitutive absence of C3aR signaling in mice leads to neurodevelopmental abnormalities that persist into adulthood and are associated with locomotive hyperactivity and altered cognitive functions.]]> Fri 27 May 2022 13:50:26 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47354 Fri 13 Jan 2023 13:20:00 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41794 Fri 12 Aug 2022 12:17:18 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51514 Fri 08 Sep 2023 12:03:44 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:37036 Fri 03 Dec 2021 10:32:41 AEDT ]]>