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Neuroprotection by a selective estrogen receptor agonist in a mouse model of global ischemia

¹Wellcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, Division of Clinical Neuroscience, University of Glasgow, Glasgow, G61 1QH; and ²Division of Neuroscience, University of Edinburgh, Edinburgh, EH8 9JZ United Kingdom

Submitted 18 March 2004 ; accepted in final form 12 May 2004

The present study employs selective estrogen receptor (ER) agonists to determine whether 17-estradiol-induced neuroprotection in global ischemia is receptor mediated and, if so, which subtype of receptor (ER or ER) is predominantly responsible. Halothane-anesthetized female C57Bl/6J mice were ovariectomized, and osmotic minipumps containing ER agonist diarylpropiolnitrile (DPN) (8 mg·kg^–1·day^–1, n = 12) or vehicle (50% DMSO in 0.9% saline) (n = 9) or ER agonist propyl pyrazole triol (PPT) (2 mg·kg^–1·day^–1, n = 13) or vehicle (50% DMSO in 0.9% saline) (n = 10) were implanted subcutaneously. One week later transient global ischemia was induced by bilateral carotid artery occlusion under halothane anesthesia, and the mice were perfusion fixed 72 h later. ER agonist DPN significantly reduced ischemic damage by 70% in the caudate nucleus and 55% in the CA1 region compared with vehicle controls (P < 0.05, Mann-Whitney U-statistic). In contrast, pretreatment with the ER agonist PPT had no effect on the extent of neuronal damage compared with controls. The data indicate a significant estrogen receptor-mediated neuroprotection in a global cerebral ischemia model involving ER.

estrogen receptor subtypes; neuroprotection; diarylpropiolnitrile; propyl pyrazole triol

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