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dc.contributor.authorLemtiri-Chlieh, Fouad
dc.contributor.authorZhao, Liangfang
dc.contributor.authorKiraly, Drew D
dc.contributor.authorEipper, Betty A
dc.contributor.authorMains, Richard E
dc.contributor.authorLevine, Eric S
dc.date.accessioned2014-08-27T09:42:21Z
dc.date.available2014-08-27T09:42:21Z
dc.date.issued2011-12-20
dc.identifier.citationLemtiri-Chlieh F, Zhao L, Kiraly DD, Eipper BA, Mains RE, et al. (2011) Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity. BMC Neuroscience 12: 126. doi:10.1186/1471-2202-12-126.
dc.identifier.issn14712202
dc.identifier.pmid22182308
dc.identifier.doi10.1186/1471-2202-12-126
dc.identifier.urihttp://hdl.handle.net/10754/325249
dc.description.abstractBackground: Dendritic spines represent the postsynaptic component of the vast majority of excitatory synapses present in the mammalian forebrain. The ability of spines to rapidly alter their shape, size, number and receptor content in response to stimulation is considered to be of paramount importance during the development of synaptic plasticity. Indeed, long-term potentiation (LTP), widely believed to be a cellular correlate of learning and memory, has been repeatedly shown to induce both spine enlargement and the formation of new dendritic spines. In our studies, we focus on Kalirin-7 (Kal7), a Rho GDP/GTP exchange factor (Rho-GEF) localized to the postsynaptic density that plays a crucial role in the development and maintenance of dendritic spines both in vitro and in vivo. Previous studies have shown that mice lacking Kal7 (Kal7 KO) have decreased dendritic spine density in the hippocampus as well as focal hippocampal-dependent learning impairments.Results: We have performed a detailed electrophysiological characterization of the role of Kal7 in hippocampal synaptic plasticity. We show that loss of Kal7 results in impaired NMDA receptor-dependent LTP and long-term depression, whereas a NMDA receptor-independent form of LTP is shown to be normal in the absence of Kal7.Conclusions: These results indicate that Kal7 is an essential and selective modulator of NMDA receptor-dependent synaptic plasticity in the hippocampus. 2011 Lemtiri-Chlieh et al; licensee BioMed Central Ltd.
dc.language.isoen
dc.publisherSpringer Nature
dc.rightsThis is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
dc.rights.urihttp://creativecommons.org/licenses/by/2.0
dc.subjectguanine nucleotide exchange factor
dc.subjectkalirin 7
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectunclassified drug
dc.subjectenzyme inhibitor
dc.subjectguanine nucleotide exchange factor
dc.subjectkalirin protein, mouse
dc.subjectn methyl dextro aspartic acid receptor
dc.subjectanimal experiment
dc.subjectanimal tissue
dc.subjectbrain electrophysiology
dc.subjectcontrolled study
dc.subjecthippocampus
dc.subjectlong term depression
dc.subjectlong term potentiation
dc.subjectmouse
dc.subjectnerve cell plasticity
dc.subjectprotein depletion
dc.subjectprotein function
dc.subjectC57BL mouse
dc.subjectdendritic spine
dc.subjectdrug antagonism
dc.subjectdrug effect
dc.subjectmetabolism
dc.subjectmouse mutant
dc.subjectorgan culture technique
dc.subjectphysiology
dc.subjectsynaptic transmission
dc.subjectDendritic Spines
dc.subjectEnzyme Inhibitors
dc.subjectGuanine Nucleotide Exchange Factors
dc.subjectHippocampus
dc.subjectMice
dc.subjectMice, Inbred C57BL
dc.subjectMice, Knockout
dc.subjectNeuronal Plasticity
dc.subjectOrgan Culture Techniques
dc.subjectReceptors, N-Methyl-D-Aspartate
dc.subjectSynaptic Transmission
dc.titleKalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity
dc.typeArticle
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Division
dc.identifier.journalBMC Neuroscience
dc.identifier.pmcidPMC3261125
dc.eprint.versionPublisher's Version/PDF
dc.contributor.institutionDepartment of Neuroscience, University of Connecticut Health Center, Farmington, CT 06030, United States
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)
kaust.personLemtiri-Chlieh, Fouad
refterms.dateFOA2018-06-13T14:39:16Z
dc.date.published-online2011-12-20
dc.date.published-print2011


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This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Except where otherwise noted, this item's license is described as This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.