Loss of NeuN immunoreactivity after cerebral ischemia does not indicate neuronal cell loss: a cautionary note

Ünal-Çevik, Isın; Toprak, M. Kılınç; Gürsoy‐Özdemir, Yasemin; Gurer, Gunfer; Dalkara, Turgay

doi:10.1016/j.brainres.2004.04.032

Cited by 239 publications

(162 citation statements)

References 22 publications

Supporting

Mentioning

141

Contrasting

Unclassified

Order By: Relevance

“…NeuN and Fluoro-Jade C stainings performed to quantify the number of healthy and suffering/dying neurons revealed that cardiac arrest led to a time-dependent neuronal death in the hippocampal CA1 region beginning to be quantitatively evident between 48 (−15% of NeuN positive cells) and 72 h post injury and reaching a maximum at 7 days post injury (−65% of NeuN positive cells; Figures 1A and B). At 24 h post-global ischemia, as previously reported, 25 we observed a NeuN staining outside of the neuronal nuclei, recovering at 72-h post-global ischemia ( Figure 1D). Parallel immunostainings for tPA ( Figures 1C and D) revealed increased levels of tPA as early as 1-h post injury, culminating at 24 h. Interestingly, whereas tPA was only detected in vessels in sham operated animals ( Figures 1C and G Figure 1G).…”

Section: Resultssupporting

confidence: 89%

Stressed neurons protect themselves by a tissue-type plasminogen activator-mediated EGFR-dependent mechanism

et al. 2015

View full text Add to dashboard Cite

In the central nervous system, tissue-type plasminogen activator (tPA) has been associated with both pro-death and prosurvival actions on neurons. In most cases, this has been related to exogenous tPA. In the present study, we addressed the influence of endogenous tPA. We first observed an increased transcription of tPA following either in vivo global brain ischemia in rats or in vitro oxygen glucose deprivation (OGD) on mice and rats hippocampal slices. Hippocampal slices from tPA-deficient mice were more sensitive to OGD than wild-type slices. Pharmacological approaches targeting the known receptors of tPA revealed that only the inhibition of phosphorylation of epidermal growth factor receptors (EGFRs) prevented the neuroprotective effect of endogenous tPA. This study shows that ischemic hippocampal neurons overproduce endogenous tPA as an intend to protect themselves from ischemic death, by a mechanism involving an activation of EGFRs. Thus, strategies contributing to promote either endogenous production of tPA or its associated EGFR-linked signaling pathway may have beneficial effects following brain injuries such as stroke.

show abstract

Section: Resultssupporting

confidence: 89%

Stressed neurons protect themselves by a tissue-type plasminogen activator-mediated EGFR-dependent mechanism

et al. 2015

View full text Add to dashboard Cite

show abstract

“…Some authors have investigated the correlation between the loss of NeuN antigenicity and the neuronal loss sustained after brain injury. They found that a significant number of neurons lose their positivity but preserve their integrity, although they may no longer be viable (Unal-Cevik et al, 2004). Our results point towards that direction.…”

Section: Neuronal Densitysupporting

confidence: 58%

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

et al. 2012

View full text Add to dashboard Cite

“…indicator of neuronal cell death by possible suppression of antibody protein or loss (18). However, Collombet et al pointed out that under their experimental condition, ischemia was so mild and the period so short after ischemic insult that loss of NeuN labeling prevented exact detection of neuronal cell death (19).…”

Section: Discussionmentioning

confidence: 98%

Ginsenoside Rb1 Reduces Neurodegeneration in the Peri-infarct Area of a Thromboembolic Stroke Model in Non-human Primates

et al. 2008

View full text Add to dashboard Cite

Abstract. Ginsenoside Rb 1 (GRb 1 ), a major component of the traditional herb ginseng, has been reported to show a neuroprotective effect in a rodent ischemic model. The purpose of this study was to investigate effects of GRb 1 on early and delayed brain injuries in a non-human primate thromboembolic stroke model. Thromboembolic stroke was induced by occlusion of the middle cerebral artery by injection of an autologous blood clot into the left internal carotid artery. GRb 1 (300 µg /kg per day, i.v.) and vehicle were administered from 7 days before embolization to the day following embolization (total: 8 times). Neurological deficits were observed at 1, 6, and 24 h and at 2, 4, and 7 days after embolization. At 7 days after embolization, neuron damage in the peri-infarct area and core region were assessed by NeuN, TUNEL, and GFAP staining. GRb 1 improved the skeletal muscle coordination score of the neurologic deficits (median: GRb 1 vs vehicle = 10 vs 12, P<0.05). In the GRb 1 group, positive neurons expressed by NeuN staining were noted in the ischemic peri-infarct area, and TUNEL-and GFAP-positive cells significantly decreased, when compared with vehicle. These results demonstrated that GRb 1 ameliorated both early and delayed injuries in the thromboembolic stroke model in non-human primates.

show abstract

Loss of NeuN immunoreactivity after cerebral ischemia does not indicate neuronal cell loss: a cautionary note

Cited by 239 publications

References 22 publications

Stressed neurons protect themselves by a tissue-type plasminogen activator-mediated EGFR-dependent mechanism

Stressed neurons protect themselves by a tissue-type plasminogen activator-mediated EGFR-dependent mechanism

Effect of intracortical vascular endothelial growth factor infusion and blockade during the critical period in the rat visual cortex

Ginsenoside Rb1 Reduces Neurodegeneration in the Peri-infarct Area of a Thromboembolic Stroke Model in Non-human Primates

Contact Info

Product

Resources

About