scholarly journals Hypoxic-ischemic brain injury exacerbates neuronal apoptosis and precipitates spontaneous seizures in glucose transporter isoform 3 heterozygous null mice

2010 ◽  
Vol 88 (15) ◽  
pp. 3386-3398 ◽  
Author(s):  
Camille Fung ◽  
Edward Evans ◽  
Don Shin ◽  
Bo-Chul Shin ◽  
Yuanzi Zhao ◽  
...  
Keyword(s):  
Brain Injury ◽  
Neuronal Apoptosis ◽  
Glucose Transporter ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Spontaneous Seizures ◽  
Hypoxic Ischemic Brain Injury

Effects of caffeine on neuronal apoptosis in neonatal hypoxic-ischemic brain injury

2014 ◽  
Vol 27 (14) ◽  
pp. 1470-1475 ◽  
Author(s):  
Hasan Kilicdag ◽  
Yusuf Kenan Daglioglu ◽  
Seyda Erdogan ◽  
Suzan Zorludemir
Keyword(s):  
Brain Injury ◽  
Neuronal Apoptosis ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury

scholarly journals Role of immunoglobulin in neuronal apoptosis in a neonatal rat model of hypoxic ischemic brain injury

2014 ◽  
Vol 7 (3) ◽  
pp. 734-738 ◽  
Author(s):  
SALIH KALAY ◽  
OSMAN ÖZTEKIN ◽  
GÖNÜL TEZEL ◽  
HAKAN ALDEMIR ◽  
EMEL SAHIN ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Neuronal Apoptosis ◽  
Neonatal Rat ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Neonatal Rat Model

The effect of levetiracetam on neuronal apoptosis in neonatal rat model of hypoxic ischemic brain injury

2013 ◽  
Vol 89 (5) ◽  
pp. 355-360 ◽  
Author(s):  
Hasan Kilicdag ◽  
Kenan Daglıoglu ◽  
Seyda Erdogan ◽  
Aslan Guzel ◽  
Leman Sencar ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Neuronal Apoptosis ◽  
Neonatal Rat ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Neonatal Rat Model

The role of trapidil on neuronal apoptosis in neonatal rat model of hypoxic ischemic brain injury

2008 ◽  
Vol 84 (4) ◽  
pp. 243-247 ◽  
Author(s):  
Aytug Atici ◽  
Gulcin Bozlu ◽  
Ali Haydar Turhan ◽  
Ayse Polat ◽  
Ali Nayci ◽  
...  
Keyword(s):  
Brain Injury ◽  
Rat Model ◽  
Neuronal Apoptosis ◽  
Neonatal Rat ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Hypoxic Ischemic Brain Injury ◽  
Neonatal Rat Model

Postnatal hypoxic-ischemic brain injury alters mechanisms mediating neuronal glucose transport

2004 ◽  
Vol 286 (2) ◽  
pp. R273-R282 ◽  
Author(s):  
Ann Zovein ◽  
Judy Flowers-Ziegler ◽  
Shanthie Thamotharan ◽  
Don Shin ◽  
Raman Sankar ◽  
...  
Keyword(s):  
Brain Injury ◽  
Glucose Uptake ◽  
Glucose Transporter ◽  
Synapsin I ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Brain Glucose ◽  
Modest Increase ◽  
Hypoxic Ischemia ◽  
Hypoxic Ischemic Brain Injury

We examined the effect of hypoxic ischemia and hypoxia vs. normoxia on postnatal murine brain substrate transporter concentrations and function. We detected a transient increase in the neuronal brain glucose transporter isoform (GLUT-3) in response to hypoxic ischemia after 4 h of reoxygenation. This increase was associated with no change in GLUT-1 (blood-brain barrier/glial isoform), monocarboxylate transporter isoforms 1 and 2, synapsin I (neuronal marker), or Bax (proapoptotic protein) but with a modest increase in Bcl-2 (antiapoptotic mitochondrial protein) protein concentrations. At 24 h of reoxygenation, the increase in GLUT-3 disappeared but was associated with a decline in Bcl-2 protein concentrations and the Bcl2:Bax ratio, an increase in caspase-3 enzyme activity (apoptotic effector enzyme), and extensive DNA fragmentation, which persisted later in time (48 h) only in the hippocampus. Hypoxia alone in the absence of ischemia was associated with a transient but modest increase in GLUT-3 and synapsin I protein concentrations, which did not cause significant apoptosis and/or necrosis. Assessment of glucose transporter function by 2-deoxyglucose (2-DG) uptake using two distinct techniques, namely positron emission tomography (PET) and the modified Sokoloff method, revealed a discrepancy due to glucose uptake by extracranial Harderian glands that masked the accurate detection of intracranial brain glucose uptake by PET scanning. The modified Sokoloff method assessing 2-DG uptake revealed that the transient increase in GLUT-3 was critical in protecting against a decline in brain glucose uptake. We conclude that hypoxic-ischemic brain injury is associated with transient compensatory changes targeted at protecting glucose delivery to fuel cellular energy metabolism, which then may delay the processes of apoptosis and cell necrosis.

Trace Fear Conditioning Detects Hypoxic-Ischemic Brain Injury in Neonatal Mice

2011 ◽  
Vol 33 (3-4) ◽  
pp. 222-230 ◽  
Author(s):  
Katarina Järlestedt ◽  
Alison L. Atkins ◽  
Henrik Hagberg ◽  
Marcela Pekna ◽  
Carina Mallard
Keyword(s):  
Brain Injury ◽  
Fear Conditioning ◽  
Ischemic Brain Injury ◽  
Ischemic Brain ◽  
Neonatal Mice ◽  
Trace Fear Conditioning ◽  
Hypoxic Ischemic Brain Injury ◽  
Trace Fear
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