Ablation of NMDA Receptors Enhances the Excitability of Hippocampal CA3 Neurons 英文参考文献.docVIP

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Ablation of NMDA Receptors Enhances the Excitability of Hippocampal CA3 Neurons 英文参考文献.doc

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Ablation of NMDA Receptors Enhances the Excitability of Hippocampal CA3 Neurons 英文参考文献

AblationofNMDAReceptorsEnhancestheExcitabilityof HippocampalCA3Neurons FumiakiFukushima1,KazuhitoNakao1,ToruShinoe2¤a,MasahiroFukaya3,Shin-ichiMuramatsu4 ,Kenji Sakimura5,HirotakaKataoka1,HisashiMori1¤b,MasahikoWatanabe3,ToshiyaManabe2,6 ,Masayoshi Mishina1* 1DepartmentofMolecularNeurobiologyandPharmacology,GraduateSchoolofMedicine,UniversityofTokyo,Tokyo,Japan,2DivisionofNeuronalNetwork,Instituteof Medical Science, University of Tokyo, Tokyo, Japan, 3Department of Anatomy, Hokkaido University School of Medicine, Sapporo, Japan, 4Division of Neurology, Department of Medicine, Jichi Medical University, Tochigi, Japan, 5Department of Cellular Neurobiology, Brain Research Institute, Niigata University, Niigata, Japan, 6CREST,JST,Kawaguchi,Japan Abstract SynchronizeddischargesinthehippocampalCA3recurrentnetworkaresupposedtounderlienetworkoscillations,memory formation and seizure generation. In the hippocampal CA3 network, NMDA receptors are abundant at the recurrent synapsesbutscarceatthemossyfibersynapses.WegeneratedmutantmiceinwhichNMDAreceptorswereabolishedin hippocampal CA3 pyramidal neurons by postnatal day 14. The histological and cytological organizations of the hippocampal CA3region were indistinguishable between control andmutant mice. We found that mutant mice lacking NMDAreceptorsselectivelyinCA3pyramidalneuronsbecamemoresusceptibletokainate-inducedseizures.Consistently, mutantmiceshowedcharacteristiclargeEEGspikesassociatedwithmultipleunitactivities(MUA), suggestingenhanced synchronous firing of CA3 neurons. The electrophysiological balance between fast excitatory and inhibitory synaptic transmissionwascomparablebetweencontrolandmutantpyramidalneuronsinthehippocampalCA3region,whilethe NMDAreceptor-slowAHPcouplingwasdiminishedinthemutantneurons.Intheadultbrain,inducibleablationofNMDA receptorsinthehippocampalCA3regionbytheviralexpressionvectorforCrerecombinasealsoinducedsimilarlargeEEG spikes. Furthermore, pharmacological blockade of CA3 NMDA recept