English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse
  1. View item / 
  2. Item Summary

Item

ITEM ACTIONSEXPORT
Add to Basket
  Local TagsRelease HistoryDetailsSummary

Released
Journal Article

Endothelin B receptor deficiency augments neuronal damage upon exposure to hypoxia-ischemia in vivo

MPS-Authors

Sirén,  Anna Leena
Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182276

Lewczuk,  Pjotr
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

Hasselblatt,  M.
Max Planck Institute of Experimental Medicine, Max Planck Society;

Dembowski,  C.
Max Planck Institute of Experimental Medicine, Max Planck Society;

/persons/resource/persons182138

Ehrenreich,  Hannelore
Clinical neuroscience, Max Planck Institute of Experimental Medicine, Max Planck Society;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

Sirén, A. L., Lewczuk, P., Hasselblatt, M., Dembowski, C., Schilling, L., & Ehrenreich, H. (2002). Endothelin B receptor deficiency augments neuronal damage upon exposure to hypoxia-ischemia in vivo. Brain Research, 945(1), 144-149.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0029-18EB-0
Abstract
The role of functional endothelin-B (ETB)-receptors on neuronal survival upon hypoxia-ischemia (HI) has been investigated in 14-day-old ETB-receptor-deficient spotting lethal (sl/sl) and wildtype (+/+) rats. Carotid ligation followed by exposure to 8% oxygen for 2 h produced distinct cortical and hippocampal neuronal damage. Damage severity 24 h after HI was mild to intermediate in +/+ rats whereas large cortical infarcts and profound apoptosis of the hippocampus evolved in sl/sl rats. The number of apoptotic cells in the dentate 24 h after HI amounted to 30+/-7 cells/0.1 mm(2) in sl/sl compared to 9+/- 3cells/0.1 mm(2) in wildtype rats (mean+/-S.E.M., n=10-11, P=0.0093). In-vitro hypoxia (15 h) resulted in a comparable increase in cell death in primary pure neuronal hippocampal cultures from both groups (49.8+/-1.6% in sl/sl, 51.4+/-0.9% in +/+, mean+/-S.E.M., n=5, P=0.0560). To conclude, absence of functional ETB receptors is associated with an increased susceptibility to HI in-vivo, which is not intrinsic to neurons. Antagonism of ETB receptors seems not to be desirable in ischemic stroke. (C) 2002 Elsevier Science B.V. All rights reserved.