Acute administration of non-classical estrogen receptor agonists attenuates ischemia-induced hippocampal neuron loss in middle-aged female rats.

Background: Pretreatment with 17beta-estradiol (E2) is profoundly neuroprotective in young animals subjected to focal and global ischemia. However, whether E2 retains its neuroprotective efficacy in aging animals, especially when administered after brain insult, is largely unknown.

Methodology/principal Findings: We examined the neuroprotective effects of E2 and two agonists that bind to non-classical estrogen receptors, G1 and STX, when administered after ischemia in middle-aged rats after prolonged ovarian hormone withdrawal.

Spontaneous temperature changes in the 2-vessel occlusion model of cerebral ischemia in rats.

Transient global ischemia (ISC) in rats and humans causes selective and delayed neuronal death in the hippocampal CA1 sector. It is clear from rodent studies that hyperthermia aggravates, whereas hypothermia lessens, this injury. In this study we sought to relate core (Tc) and brain (Tb) temperature, measured via telemetry probes, after ISC produced in rats by bilateral common carotid artery occlusion combined with systemic hypotension (2-VO model).

Failure of estradiol to ameliorate global ischemia-induced CA1 sector injury in middle-aged female gerbils.

Global forebrain ischemia arising from brief occlusion of the carotid arteries in gerbils produces selective hippocampal CA1 neuronal loss. Pre-treatment with 17beta-estradiol ameliorates, in part, ischemia-induced damage in young animals. Because stroke and cardiac arrest are more likely to occur among elderly individuals, neuroprotective studies in older animals have compelling clinical relevance.