Comparison of different quantification methods to determine hippocampal damage after cerebral ischemia

Wang, Jie; Jahn‐Eimermacher, Antje; Brückner, Melanie; Werner, Christian; Engelhard, Kristin; Thal, Serge C.

doi:10.1016/j.jneumeth.2014.11.001

Cited by 15 publications

(11 citation statements)

References 30 publications

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“…Therefore results are likely to differ between both methods, depending on the time at which brains were harvested after the insult. Such differences between staining methods have been reported previously, although in different models (33,34). The trend in the CV staining show in the same direction as the FJB staining, which supports our results.…”

Section: The P53 Protein and Its Products Have A Central Role In Apopsupporting

confidence: 92%

Neuroprotection with the P53-Inhibitor Pifithrin-μ after Cardiac Arrest in a Rodent Model

Glas

Frick

Springe

et al. 2018

Shock

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Section: The P53 Protein and Its Products Have A Central Role In Apopsupporting

confidence: 92%

Neuroprotection with the P53-Inhibitor Pifithrin-μ after Cardiac Arrest in a Rodent Model

Glas

Frick

Springe

et al. 2018

Shock

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“…Our results indicated that within first 24 hr of reperfusion, the registered decrease in NeuN staining was not statistically significant. According to the literature, immunostaining for NeuN that detected loss of CA1 neurons in hippocampus occurs 2-4 days after global cerebral ischaemia [45,46] while Zhou et al [47] did not find significant CA1 neuronal loss within 10 weeks after 2-hr MCAO in comparison with the control animals. In conclusion, within first 24 hr after 1-hr MCAO, there was no significant neuronal loss of the hippocampal tissue.…”

Section: Discussionmentioning

confidence: 99%

Decrease in Oxidative Stress Parameters after Post‐Ischaemic Recombinant Human Erythropoietin Administration in the Hippocampus of Rats Exposed to Focal Cerebral Ischaemia

Mršić-Pelčić

Pilipović

Pelčić

et al. 2017

Basic Clin Pharma Tox

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Recombinant human erythropoietin (rhEpo) is a multi-functional drug with antioxidant potential. However, the underlying molecular mechanisms of its action are still unclear. The purpose of this study was to investigate the effects of rhEpo on the brain infarct volume as well as on the levels of the neuronal damage, oxidative stress parameters and active caspase-3, nuclear factor erythroid 2-related factor 2 (Nrf2) and haemeoxygenase-1 (HO-1) expressions in the hippocampi of rats exposed to the right middle cerebral artery occlusion (MCAO) for 1 hr. Ischaemic animals received either vehicle or rhEpo (5000 IU/kg, i.p.) immediately or 3 hr after the induction of ischaemia. Sham-operated, vehicle-treated animals served as the control group. Rats were killed 24 hr after the onset of the ischaemic or sham experimental procedure. MCAO caused ipsilateral brain infarction within the striatum and cortex. In the CA1 region of the hippocampi, we did not find significant neuronal loss, but a statistically significant rise in the active caspase-3 and Nrf2 protein expressions was registered. We detected also significant increases in the hippocampal levels of oxidative stress parameters (thiobarbituric acid-reactive substances, superoxide dismutase, glutathione peroxidase). Post-ischaemic administration of rhEpo significantly reduced the brain infarct volume, decreased levels of all tested oxidative stress parameters and increased the Nrf2 expression level. These findings suggest that decrease in oxidative stress parameters in the hippocampus could be an early indicator of post-ischaemic neuroprotective effect of rhEpo in rats exposed to focal cerebral ischaemia and that this effect could be attributable to additional post-ischaemic activation of Nrf2 endogenous antioxidant system.

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“…We then asked if this defective glial scar development affects surrounding neurons. Loss of NeuN indicates degenerating neurons (Alekseeva et al, 2015), and its translocation from the nucleus to the cytosol identifies neurons exhibiting an initial stress response to pathologies (Lucas et al, 2014;Shandra et al, 2019;Wang et al, 2015;Wiley et al, 2016). Following stab injury, WT brains consistently maintained NeuN in the neuronal nuclei irrespective of their position relative to the injury site.…”

Section: Reactive Astrocytes Require Dbn To Form Glia Scars In Vivomentioning

confidence: 99%

Drebrin mediates scar formation and astrocyte reactivity during brain injury by inducing RAB8 tubular endosomes

Schiweck

Murk

Ledderose

et al. 2020

Preprint

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The brain of mammals lacks a significant ability to regenerate neurons and is thus particularly vulnerable. To protect the brain from injury and disease, damage control by astrocytes through astrogliosis and scar formation is vital. Here, we show that brain injury triggers an ad hoc upregulation of the actin-binding protein Drebrin (DBN) in astrocytes, which is essential for the formation and maintenance of glial scars in vivo. In turn, DBN loss leads to defective glial scar formation and excessive neurodegeneration following mild brain injuries. At the cellular level, DBN switches actin homeostasis from ARP2/3-dependent arrays to microtubule-compatible scaffolds and facilitates the formation of RAB8-positive membrane tubules. This injury-specific RAB8 membrane compartment serves as hub for the trafficking of surface proteins involved in astrogliosis and adhesive responses, such as β1integrin. Our work identifies DBN as pathology-specific actin regulator, and establishes DBNdependent membrane trafficking as crucial mechanism in protecting the brain from escalating damage following traumatic injuries. MAINThe brain of higher mammals is vulnerable to traumatic injury and disease, but largely lacks the capacity to regenerate neurons and rarely regains function in damaged areas (Barker et al., 2018). This makes the containment of local pathological incidents critical to avoid the propagation of inflammation and neurodegeneration into the uninjured brain parenchyma.Astrocytes are key players in protection of CNS tissue via a defense mechanism known as reactive astrogliosis. This process is associated with comprehensive changes in astrocyte morphology and function (Schiweck et al., 2018). Reactive astrocytes develop hypertrophies of soma and protrusions, while cells in proximity to large lesion sites polarize and extend particularly long processes. Dense arrays of such 'palisades' and hypertrophic astrocytes constitute glial scars, which enclose as physical barriers inflammatory cues and extravasating leucocytes, and limit the spread of damage (Faulkner et al., 2004;Frik et al., 2018). Glial scars are anatomically well described, but the molecular details controlling astrocyte reactivity are still poorly understood.In the context of astrogliosis and scar formation, we studied drebrin (DBN), a cytoskeletal regulator, which stabilizes actin filaments by sidewise binding and by competing off other actin binding proteins (Grintsevich et al., 2010;Mikati et al., 2013). It is widely expressed, but has mainly been studied in neurons (Aoki et al., 2005). In cultured astrocytes, DBN has been described to maintain connexin 43 at the plasma membrane (Butkevich et al., 2004).Functional coupling of astrocytes into networks through gap junctions is essential to modulate neuronal transmission (He et al., 2020;Pannasch and Rouach, 2013). A deficit in DBN would therefore be expected to cause profound phenotypes in vivo. However, mouse models with acute or chronic DBN loss indicate non-essential functions of this actin binding protein d...

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Comparison of different quantification methods to determine hippocampal damage after cerebral ischemia

Cited by 15 publications

References 30 publications

Neuroprotection with the P53-Inhibitor Pifithrin-μ after Cardiac Arrest in a Rodent Model

Neuroprotection with the P53-Inhibitor Pifithrin-μ after Cardiac Arrest in a Rodent Model

Decrease in Oxidative Stress Parameters after Post‐Ischaemic Recombinant Human Erythropoietin Administration in the Hippocampus of Rats Exposed to Focal Cerebral Ischaemia

Drebrin mediates scar formation and astrocyte reactivity during brain injury by inducing RAB8 tubular endosomes

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