scholarly journals Insights into cytoprotection from ground squirrel hibernation, a natural model of tolerance to profound brain oligaemia

2006 ◽  
Vol 34 (6) ◽  
pp. 1295-1298 ◽  
Author(s):  
Y.-J. Lee ◽  
J.M. Hallenbeck
Keyword(s):  
Signal Transduction ◽  
Blood Flow ◽  
Brain Damage ◽  
Oxygen Delivery ◽  
Ground Squirrel ◽  
Signal Transduction Pathways ◽  
Post Translational Modification ◽  
Ischaemic Brain ◽  
Ischaemic Brain Damage ◽  
Natural Tolerance

Progression of acute ischaemic brain damage is complex and multifactorial. Also, evidence suggests that participating molecules and signal transduction pathways can function differently in different cellular contexts. Hibernation torpor, a model of natural tolerance to profoundly reduced blood flow and oxygen delivery to brain, along with models of induced ischaemic tolerance can guide efforts to identify cytoprotective mechanisms that are multifactorial and that target multiple mechanisms in multiple cellular contexts. Post-translational modification of proteins by conjugation with the SUMO (small ubiquitin-related modifier) is massively increased in hibernation and may be such a mechanism.

Spatiotemporal differences in vascular permeability after ischaemic brain damage

Neuroreport ◽  
2011 ◽  
Vol 22 (9) ◽  
pp. 424-427 ◽  
Author(s):  
Masato Yano ◽  
Naoyuki Kawao ◽  
Yukinori Tamura ◽  
Kiyotaka Okada ◽  
Shigeru Ueshima ◽  
...  
Keyword(s):  
Vascular Permeability ◽  
Brain Damage ◽  
Ischaemic Brain ◽  
Ischaemic Brain Damage

Ischaemic Brain Damage Induced by Rapid Lowering of Arterial Pressure in Hypertension

1984 ◽  
Vol 2 (3) ◽  
pp. 297???304 ◽  
Author(s):  
David I. Graham ◽  
Anne McGeorge ◽  
William Fitch ◽  
John V. Jones ◽  
Eric T. MacKenzie
Keyword(s):  
Arterial Pressure ◽  
Brain Damage ◽  
Ischaemic Brain ◽  
Ischaemic Brain Damage

NF-κB signalling in cerebral ischaemia

2006 ◽  
Vol 34 (6) ◽  
pp. 1291-1294 ◽  
Author(s):  
M. Schwaninger ◽  
I. Inta ◽  
O. Herrmann
Keyword(s):  
Infarct Size ◽  
Brain Damage ◽  
Cerebral Ischaemia ◽  
Neuronal Cell ◽  
Tissue Loss ◽  
Ischaemic Brain ◽  
Ischaemic Brain Damage ◽  
On The Road ◽  
Apoptosis And Inflammation

In acute stroke, neuronal apoptosis and inflammation are considered to be important mechanisms on the road to tissue loss and neurological deficit. Both apoptosis and inflammation depend on gene transcription. We have identified a signalling pathway that regulates transcription of genes involved in apoptosis and inflammation. In a mouse model of focal cerebral ischaemia, there is an induction of the cytokine TWEAK (tumour necrosis factor-like weak inducer of apoptosis) and its membrane receptor Fn14. TWEAK promotes neuronal cell death and activates the transcription factor NF-κB (nuclear factor κB) through the upstream kinase IKK [IκB (inhibitory κB) kinase]. In vivo, IKK is activated in neurons. Neuron-specific deletion of the subunit IKK2 or inhibition of IKK activity reduced the infarct size and neuronal cell loss. A pharmacological inhibitor of IKK also showed neuroprotective properties. IKK-dependent ischaemic brain damage is likely to be mediated by NF-κB, because neuron-specific inhibition of NF-κB through transgenic expression of the NF-κB superrepressor was found to reduce the infarct size. In summary, there is evidence that IKK/NF-κB signalling contributes to ischaemic brain damage and may provide suitable drug targets for the treatment of stroke.

scholarly journals ISCHAEMIC BRAIN DAMAGE: THE ROLE OF EXCITATORY ACTIVITY AND OF CALCIUM ENTRY

1985 ◽  
Vol 57 (1) ◽  
pp. 44-46 ◽  
Author(s):  
B. MELDRUM ◽  
M. EVANS ◽  
T. GRIFFITHS ◽  
R. SIMON
Keyword(s):  
Brain Damage ◽  
Calcium Entry ◽  
Ischaemic Brain ◽  
Excitatory Activity ◽  
Ischaemic Brain Damage

Erratum

1994 ◽  
Vol 14 (5) ◽  
pp. 884-884
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Ground Squirrel ◽  
Weighted Average ◽  
Ground Squirrels ◽  
Control Group ◽  
Local Cerebral Blood Flow ◽  
Correct Number ◽  
Natural Tolerance ◽  
The Brain

Local Cerebral Blood Flow During Hibernation, a Model of Natural Tolerance to “Cerebral Ischemia” Kai U. Frerichs, Charles Kennedy, Louis Sokoloff and John M. Hallenbeck [ originally published in Journal of Cerebral Blood Flow and Metabolism 1994;14(2):193–205] The weighted average cerebral blood flow in the brains of hibernating and nonhibernating ground squirrels appeared in three places in the article cited above. The numbers varied to some extent in each of the three places that they were displayed. The correct number for the active ground squirrel group was 62 ± 18 ml 100 g−1 min−1. The correct number for the hibernating group was 7 ± 4 ml 100 g−1 min−1. These numbers should be inserted on page 193 in the abstract so that the sentence would read, “Mean (± SD) mass-weighted CBF in the brain was 62 ± 18 ml 100 g−1 min−1 (n = 4) in the control group but was reduced to ischemic levels, 7 ± 4 ml 100 g−1 min−1 (n = 4), in the hibernating animals (p < 0.001).” The same numbers should be inserted into the sentence that begins at the bottom of page 198, “Average blood flow (± SD) in the brain as a whole in the hibernating animals was reduced to about 1/10 (7 ± 4 ml 100 g−1 min−1) of the level in active animals (62 ± 18 ml 100 g−1 min−1) (Table 4).” Finally, on page 201 at the bottom of Table 4 below “Weighted average in brain as a whole,” the readings should be 62 ± 18 for active and 7 ± 4 for hibernating.

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