Galanin Receptor 1 Deletion Exacerbates Hippocampal Neuronal Loss after Systemic Kainate Administration in Mice 英文参考文献.docVIP

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Galanin Receptor 1 Deletion Exacerbates Hippocampal Neuronal Loss after Systemic Kainate Administration in Mice 英文参考文献.doc

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Galanin Receptor 1 Deletion Exacerbates Hippocampal Neuronal Loss after Systemic Kainate Administration in Mice 英文参考文献

GalaninReceptor1DeletionExacerbatesHippocampal NeuronalLossafterSystemicKainateAdministrationin Mice P.ElyseSchauwecker* DepartmentofCellandNeurobiology,UniversityofSouthernCaliforniaKeckSchoolofMedicine,LosAngeles,California,UnitedStatesofAmerica Abstract Background:Galaninisaneuropeptidewithawidedistributioninthecentralandperipheralnervoussystemsandwhose physiological effects are mediated through three G protein-coupled receptor subtypes, GalR1, GalR2, and GalR3. Several linesofevidenceindicatethatgalanin,aswellasactivationoftheGalR1receptor,isapotentandeffectivemodulatorof neuronalexcitabilityinthehippocampus. Methodology/Principal Findings: In order to test more formally the potential influence of GalR1 on seizure-induced excitotoxic cell death, we conducted functional complementation tests in which transgenic mice that exhibit decreased expressionoftheGalR1candidatemRNAunderwentkainate-inducedstatusepilepticustodetermineifthequantitativetrait ofsusceptibilitytoseizure-inducedcelldeathisdeterminedbytheactivityofGalR1.Inthepresentstudy,wereportthat reductionofGalR1mRNAvianullmutationorinjectionoftheGalR1antagonist,galantide,priortokainate-inducedstatus epilepticusinduceshippocampaldamageinamousestrainknowntobehighlyresistanttokainate-inducedneuronalinjury. Wild-typeandGalR1knockoutmiceweresubjectedtosystemickainateadministration.Sevendayslater,NisslandNeuN immune-stainingdemonstratedthathippocampalcelldeathwassignificantlyincreasedinGalR1knockoutstrainsandin animals injected with the GalR1 antagonist. Compared to GalR1-expressing mice, GalR1-deficient mice had significantly largerhippocampallesionsafterstatusepilepticus. Conclusions/Significance:OurresultssuggestthatareductionofGalR1expressionintheC57BL/6Jmousestrainrenders themsusceptibletoexcitotoxicinjuryfollowingsystemickainateadministration.Fromtheseresults,GalR1proteinemerges asanewmoleculartargetthatmayhaveapotentialtherapeuticvalueinmodulatingseizure-inducedcelldeath. Citation: Schauwecker PE (2010) Gal