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Am J Physiol Heart Circ Physiol (May 20, 2004). doi:10.1152/ajpheart.00227.2004
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Submitted on March 8, 2004
Accepted on May 12, 2004

Neuroprotection by a selective oestrogen receptor {beta} agonist in a mouse model of global ischaemia

H. V.O. Carswell1*, I. M. Macrae1, L. Gallagher1, E. Harrop1, and K. J. Horsburgh2

1 Wellcome Surgical Institute & Hugh Fraser Neuroscience Labs., Division of Clinical Neuroscience, University of Glasgow, Glasgow, Scotland, United Kingdom
2 Division of Neuroscience, University of Edinburgh, Edinburgh, Scotland, United Kingdom

* To whom correspondence should be addressed. E-mail: hvo1a{at}udcf.gla.ac.uk.

The present study employs selective oestrogen receptor (ER) agonists to determine whether 17{beta}-oestradiol-induced neuroprotection in global ischaemia is receptor mediated and, if so, which subtype of receptor (ER{alpha} or ER{beta}) is predominantly responsible. Halothane anaesthetised female C57Bl/6J mice were ovariectomised and osmotic minipumps containing ER{beta} agonist diarylpropiolnitrile (DPN) (8mg/kg/day, n=12) or vehicle (50% DMSO in 0.9% saline) (n=9) or ER{alpha}agonist propyl pyrazole triol (PPT) (2mg/kg/day, n=13) or vehicle (50% DMSO in 0.9 % saline) (n=10) were implanted subcutaneously. One week later transient global ischaemia was induced by bilateral carotid artery occlusion under halothane anaesthesia and the mice perfusionfixed 72hr later. ER{beta} agonist, DPN, significantly reduced ischaemic damage by 70% in the caudate nucleus and 55% in the CA1 region as compared to vehicle controls (p<0.05, Mann Whitney U-statistic). In contrast, pretreatment with the ER{alpha} agonist PPT had no effect on the extent of neuronal damage as compared to controls. The data indicate a significant oestrogen receptor mediated neuroprotection, in a global cerebral ischaemia model involving ER{beta}.




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