Acute Administration of Non-Classical Estrogen Receptor Agonists Attenuates Ischemia-Induced Hippocampal Neuron Loss in Middle-Aged Female Rats 英文参考文献.docVIP

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Acute Administration of Non-Classical Estrogen Receptor Agonists Attenuates Ischemia-Induced Hippocampal Neuron Loss in Middle-Aged Female Rats 英文参考文献.doc

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Acute Administration of Non-Classical Estrogen Receptor Agonists Attenuates Ischemia-Induced Hippocampal Neuron Loss in Middle-Aged Female Rats 英文参考文献

AcuteAdministrationofNon-ClassicalEstrogenReceptor AgonistsAttenuatesIschemia-InducedHippocampal NeuronLossinMiddle-AgedFemaleRats DianeLebesgue1,MichaelTraub2,MaxineDeButte-Smith1,ChristopherChen1,R.SuzanneZukin1, MartinJ.Kelly3,AnneM.Etgen1* 1Dominick P. Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, New York, United States of America, 2Department of Obstetrics GynecologyandWomen’sHealth,AlbertEinsteinCollegeofMedicine,Bronx,NewYork,UnitedStatesofAmerica,3DepartmentofPhysiologyandPharmacology,Oregon HealthScienceUniversity,Portland,Oregon Abstract Background:Pretreatmentwith17b-estradiol(E2)isprofoundlyneuroprotectiveinyounganimalssubjectedtofocaland globalischemia.However,whetherE2retainsitsneuroprotectiveefficacyinaginganimals,especiallywhenadministered afterbraininsult,islargelyunknown. 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 hormonewithdrawal.Eightweeksafterovariectomy,middle-agedfemaleratsunderwent10minutesofglobalischemiaby fourvesselocclusion.Immediatelyafterreperfusion,animalsreceivedasingleinfusionofeitherE2(2.25mg),G1(50mg)or STX(50mg)intothelateralventricle(ICV)orasinglesystemicinjectionofE2(100mg/kg).Survivingpyramidalneuronsin thehippocampalCA1werequantified1weeklater.E2andbothagoniststhattargetnon-classicalestrogenreceptors(G1 andSTX)administeredICVatthetimeofreperfusionprovidedsignificantlevelsofneuroprotection,with55–60%ofCA1 neurons surviving vs 15% survival in controls. A single systemic injection of a pharmacological dose of E2 also rescued approximately50%ofCA1pyramidalneuronsdestinedtodie.TodetermineifE2andG1havesimilarmechanismsofaction inhippocampalneurons,wecomparedtheabilityofE2andG1tomodifyCA1pyramidalneuronresponsestoexcitatory inputs from the Schaffer collaterals recorded in hippocampal slices derived from female