Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity

Handle URI:
http://hdl.handle.net/10754/325249
Title:
Kalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticity
Authors:
Lemtiri-Chlieh, Fouad ( 0000-0002-7418-2623 ) ; Zhao, Liangfang; Kiraly, Drew D; Eipper, Betty A; Mains, Richard E; Levine, Eric S
Abstract:
Background: 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.
KAUST Department:
Biological and Environmental Sciences and Engineering (BESE) Division
Citation:
Lemtiri-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.
Publisher:
Springer Nature
Journal:
BMC Neuroscience
Issue Date:
19-Dec-2011
DOI:
10.1186/1471-2202-12-126
PubMed ID:
22182308
PubMed Central ID:
PMC3261125
Type:
Article
ISSN:
14712202
Appears in Collections:
Articles; Biological and Environmental Sciences and Engineering (BESE) Division

Full metadata record

DC FieldValue Language
dc.contributor.authorLemtiri-Chlieh, Fouaden
dc.contributor.authorZhao, Liangfangen
dc.contributor.authorKiraly, Drew Den
dc.contributor.authorEipper, Betty Aen
dc.contributor.authorMains, Richard Een
dc.contributor.authorLevine, Eric Sen
dc.date.accessioned2014-08-27T09:42:21Zen
dc.date.available2014-08-27T09:42:21Zen
dc.date.issued2011-12-19en
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.en
dc.identifier.issn14712202en
dc.identifier.pmid22182308en
dc.identifier.doi10.1186/1471-2202-12-126en
dc.identifier.urihttp://hdl.handle.net/10754/325249en
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.en
dc.language.isoenen
dc.publisherSpringer Natureen
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.en
dc.rights.urihttp://creativecommons.org/licenses/by/2.0en
dc.subjectguanine nucleotide exchange factoren
dc.subjectkalirin 7en
dc.subjectn methyl dextro aspartic acid receptoren
dc.subjectunclassified drugen
dc.subjectenzyme inhibitoren
dc.subjectguanine nucleotide exchange factoren
dc.subjectkalirin protein, mouseen
dc.subjectn methyl dextro aspartic acid receptoren
dc.subjectanimal experimenten
dc.subjectanimal tissueen
dc.subjectbrain electrophysiologyen
dc.subjectcontrolled studyen
dc.subjecthippocampusen
dc.subjectlong term depressionen
dc.subjectlong term potentiationen
dc.subjectmouseen
dc.subjectnerve cell plasticityen
dc.subjectprotein depletionen
dc.subjectprotein functionen
dc.subjectC57BL mouseen
dc.subjectdendritic spineen
dc.subjectdrug antagonismen
dc.subjectdrug effecten
dc.subjectmetabolismen
dc.subjectmouse mutanten
dc.subjectorgan culture techniqueen
dc.subjectphysiologyen
dc.subjectsynaptic transmissionen
dc.subjectDendritic Spinesen
dc.subjectEnzyme Inhibitorsen
dc.subjectGuanine Nucleotide Exchange Factorsen
dc.subjectHippocampusen
dc.subjectMiceen
dc.subjectMice, Inbred C57BLen
dc.subjectMice, Knockouten
dc.subjectNeuronal Plasticityen
dc.subjectOrgan Culture Techniquesen
dc.subjectReceptors, N-Methyl-D-Aspartateen
dc.subjectSynaptic Transmissionen
dc.titleKalirin-7 is necessary for normal NMDA receptor-dependent synaptic plasticityen
dc.typeArticleen
dc.contributor.departmentBiological and Environmental Sciences and Engineering (BESE) Divisionen
dc.identifier.journalBMC Neuroscienceen
dc.identifier.pmcidPMC3261125en
dc.eprint.versionPublisher's Version/PDFen
dc.contributor.institutionDepartment of Neuroscience, University of Connecticut Health Center, Farmington, CT 06030, United Statesen
dc.contributor.affiliationKing Abdullah University of Science and Technology (KAUST)en
kaust.authorLemtiri-Chlieh, Fouaden

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