Spreading depression increases immunohistochemical staining of glial fibrillary acidic protein

Kraig, Richard P.; Dong, Liming; Thisted, Ronald A.; Jaeger, Christine

doi:10.1523/jneurosci.11-07-02187.1991

Cited by 163 publications

(120 citation statements)

References 25 publications

(24 reference statements)

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“…Serial sections from all regions of NF1 SynI KO brains were compared to normal counterparts, and no evidence of microgliosis was found (data not shown). Taken together, these results indicate that loss of NF1 in neurons does not elicit the classical morphological features of neuronal degeneration and microgliosis but, rather, may alter normal neuronal physiology, thus exerting an effect on surrounding astrocytes (Kraig et al 1991;Steward et al 1991).…”

Section: Ko Brains Do Not Develop Neuronal Degeneration or Microgliosismentioning

confidence: 80%

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Zhu¹,

Romero²,

Ghosh³

et al. 2001

Genes Dev.

536

547

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Neurofibromatosis type 1 (NF1) is a prevalent genetic disorder that affects growth properties of neural-crest-derived cell populations. In addition, approximately one-half of NF1 patients exhibit learning disabilities. To characterize NF1 function both in vitro and in vivo, we circumvent the embryonic lethality of NF1 null mouse embryos by generating a conditional mutation in the NF1 gene using Cre/loxP technology. Introduction of a Synapsin I promoter driven Cre transgenic mouse strain into the conditional NF1 background has ablated NF1 function in most differentiated neuronal populations. These mice have abnormal development of the cerebral cortex, which suggests that NF1 has an indispensable role in this aspect of CNS development. Furthermore, although they are tumor free, these mice display extensive astrogliosis in the absence of conspicuous neurodegeneration or microgliosis. These results indicate that NF1-deficient neurons are capable of inducing reactive astrogliosis via a non-cell autonomous mechanism.

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Section: Ko Brains Do Not Develop Neuronal Degeneration or Microgliosismentioning

confidence: 80%

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Zhu¹,

Romero²,

Ghosh³

et al. 2001

Genes Dev.

536

547

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“…However, as NBO has been shown to be protective in a milder model of permanent ischemia (Veltkamp et al, 2006), we tested the hypothesis that longer ( > 3 h) treatment durations may be beneficial in the more severe suture model, and indeed, 6-h NBO treatment reduced final infarct size if initiated within 30 mins after pMCAO. In addition to blunting spreading depression (Kraig et al, 1991), oxygen may have provided lasting neuroprotection by reducing ischemiainduced cell-death pathway activation (Veltkamp et al, 2006).…”

Section: Discussionmentioning

confidence: 99%

Normobaric Hyperoxia Delays Perfusion/Diffusion Mismatch Evolution, Reduces Infarct Volume, and Differentially Affects Neuronal Cell Death Pathways after Suture Middle Cerebral Artery Occlusion in Rats

Henninger

Bouley

Nelligan

et al. 2007

J Cereb Blood Flow Metab

108

107

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Normobaric hyperoxia (NBO) has been shown to extend the reperfusion window after focal cerebral ischemia. Employing diffusion (DWI)-and perfusion (PWI)-weighted magnetic resonance imaging (MRI), the effect of NBO (100% started at 30 mins after middle cerebral artery occlusion (MCAO)) on the spatiotemporal evolution of ischemia during and after permanent (pMCAO) and transient suture middle cerebral artery occlusion (tMCAO) was investigated (experiment 3). In two additional experiments, time window (experiment 1) and cell death pathways (experiment 2) were investigated in the pMCAO model. In experiment 1, NBO treatment reduced infarct volume at 24 h after pMCAO by 10% when administered for 3 h (P > 0.05) and by 44% when administered for 6 h (P < 0.05). In experiment 2, NBO acutely (390 mins, P < 0.05) reduced in situ end labeling (ISEL) positivity in the ipsilesional penumbra but increased contralesional necrotic as well as caspase-3-mediated apoptotic cell death. In experiment 3, CBF characteristics and CBF-derived lesion volumes did not differ between treated and untreated animals, whereas the apparent diffusion coefficient (ADC)-derived lesion volume essentially stopped progressing during NBO treatment, resulting in a persistent PWI/DWI mismatch that could be salvaged by delayed (3 h) reperfusion. In conclusion, NBO (1) acutely preserved the perfusion/diffusion mismatch without altering CBF, (2) significantly extended the time window for reperfusion, (3) induced lasting neuroprotection in permanent ischemia, and (4) although capable of reducing cell death in hypoperfused tissue it also induced cell death in otherwise unaffected areas. Our data suggest that NBO may represent a promising strategy for acute stroke treatment.

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“…Although spreading depression causes no permanent neuronal injury [22], it does cause gliosis [18], indicating that spreading depression perturbs the tissue. Dark neuron formation might be stimulated by spreading depression.…”

Section: Discussionmentioning

confidence: 99%

Pharmacologic analysis of the mechanism of dark neuron production in cerebral cortex

Kherani

Auer

2008

Acta Neuropathol

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Dark neurons have plagued the interpretation of brain tissue sections, experimentally and clinically. Seen only when perturbed but living tissue is Wxed in aldehydes, their mechanism of production is unknown. Since dark neurons are seen in cortical biopsies, experimental ischemia, hypoglycemia, and epilepsy, we surmised that glutamate release and neuronal transmembrane ion Xuxes could be the perturbation leading to dark neuron formation while the Wxation process is underway. Accordingly, we excised biopsies of rat cortex to simulate neurosurgical production of dark neurons. To ascertain the role of glutamate, blockade of N-methyl-D-aspartate (NMDA) and non-NMDA receptors was done prior to formaldehyde Wxation. To assess the role of transmembrane sodium ion (and implicitly, water) Xuxes, tetraethylammonium (TEA) was used. Blockade of NMDA receptors with MK-801 and non-NMDA receptors with the quinoxalinediones (CNQX and NBQX) abolished dark neuron formation. More delayed exposure of the tissue to the antagonist, CNQX, by admixing it with the Wxative directly, allowed for some production of dark neurons. Aminophosphonoheptanoate (APH), perhaps due to its polarity, and TEA, did not prevent dark neurons, which were abundant in control formaldehyde Wxed material unexposed to either receptor or ion channelantagonists. The results demonstrate a role for the pharmacologic subtypes of glutamate receptors in the pathogenetic mechanism of dark neuron formation. Our results are consistent with the appearance of dark neurons in biopsy where the cerebral cortex has been undercut, and rendered locally ischemic and hypoglycemic, as well as in epilepsy, hypoglycemia, and ischemia, all of which lead to glutamate release. Rather than a pressure-derived mechanical origin, we suggest that depolarization, glutamate release or receptor activation are more likely mechanisms of dark neuron production.Keywords Dark neuron · Biopsy artifact · Histology · Excitatory amino acid receptor blocker · Pharmacology · NMDA receptor · APH · MK-801 · CNQX · NBQX · TEA

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Spreading depression increases immunohistochemical staining of glial fibrillary acidic protein

Cited by 163 publications

References 25 publications

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Ablation of NF1 function in neurons induces abnormal development of cerebral cortex and reactive gliosis in the brain

Normobaric Hyperoxia Delays Perfusion/Diffusion Mismatch Evolution, Reduces Infarct Volume, and Differentially Affects Neuronal Cell Death Pathways after Suture Middle Cerebral Artery Occlusion in Rats

Pharmacologic analysis of the mechanism of dark neuron production in cerebral cortex

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