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Article: Decreased Anxiety, Altered Place Learning, and Increased CA1 Basal Excitatory Synaptic Transmission in Mice with Conditional Ablation of the Neural Cell Adhesion Molecule L1

TitleDecreased Anxiety, Altered Place Learning, and Increased CA1 Basal Excitatory Synaptic Transmission in Mice with Conditional Ablation of the Neural Cell Adhesion Molecule L1
Authors
KeywordsAnxiety
Cell adhesion molecule
Hippocampus
L1
Place learning
Synaptic plasticity
Issue Date2003
PublisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.org
Citation
Journal Of Neuroscience, 2003, v. 23 n. 32, p. 10419-10432 How to Cite?
AbstractL1, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation and axon outgrowth and guidance. Mutations in the human and mouse L1 gene result in similarly severe neurological abnormalities. To dissociate the functional roles of L1 in the adult brain from developmental abnormalities, we have generated a mutant in which the L1 gene is inactivated by cre-recombinase under the control of the calcium/calmodulin-dependent kinase II 11 promoter. This mutant (L1fy+) did not show the overt morphological and behavioral abnormalities observed previously in constitutive L1-deficient (L1-/-) mice; however, there was an increase in basal excitatory synaptic transmission that was not apparent in L1-/-mice. Similar to L1-/- mice, no defects in short- and long-term potentiation in the CA1 region of the hippocampus were observed. Interestingly, L1fy+ mice showed decreased anxiety in the open field and elevated plus-maze, contrary to L1-/- mice, and altered place learning in the water maze, similar to L1-/- mice. Thus, mice conditionally deficient in L1 expression in the adult brain share some abnormalities, but also display different ones, as compared with L1-/- mice, highlighting the role of L1 in the regulation of synaptic transmission and behavior in adulthood.
Persistent Identifierhttp://hdl.handle.net/10722/53594
ISSN
2015 Impact Factor: 5.924
2015 SCImago Journal Rankings: 5.105
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLaw, JWSen_HK
dc.contributor.authorLee, AYWen_HK
dc.contributor.authorSun, Men_HK
dc.contributor.authorNikonenko, AGen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorDityatev, Aen_HK
dc.contributor.authorSchachner, Men_HK
dc.contributor.authorMorellini, Fen_HK
dc.date.accessioned2009-04-03T07:24:07Z-
dc.date.available2009-04-03T07:24:07Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of Neuroscience, 2003, v. 23 n. 32, p. 10419-10432en_HK
dc.identifier.issn0270-6474en_HK
dc.identifier.urihttp://hdl.handle.net/10722/53594-
dc.description.abstractL1, a neural cell adhesion molecule of the immunoglobulin superfamily, is involved in neuronal migration and differentiation and axon outgrowth and guidance. Mutations in the human and mouse L1 gene result in similarly severe neurological abnormalities. To dissociate the functional roles of L1 in the adult brain from developmental abnormalities, we have generated a mutant in which the L1 gene is inactivated by cre-recombinase under the control of the calcium/calmodulin-dependent kinase II 11 promoter. This mutant (L1fy+) did not show the overt morphological and behavioral abnormalities observed previously in constitutive L1-deficient (L1-/-) mice; however, there was an increase in basal excitatory synaptic transmission that was not apparent in L1-/-mice. Similar to L1-/- mice, no defects in short- and long-term potentiation in the CA1 region of the hippocampus were observed. Interestingly, L1fy+ mice showed decreased anxiety in the open field and elevated plus-maze, contrary to L1-/- mice, and altered place learning in the water maze, similar to L1-/- mice. Thus, mice conditionally deficient in L1 expression in the adult brain share some abnormalities, but also display different ones, as compared with L1-/- mice, highlighting the role of L1 in the regulation of synaptic transmission and behavior in adulthood.en_HK
dc.languageengen_HK
dc.publisherSociety for Neuroscience. The Journal's web site is located at http://www.jneurosci.orgen_HK
dc.relation.ispartofJournal of Neuroscienceen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.rightsJournal of Neuroscience. Copyright © Society for Neuroscience.en_HK
dc.subjectAnxietyen_HK
dc.subjectCell adhesion moleculeen_HK
dc.subjectHippocampusen_HK
dc.subjectL1en_HK
dc.subjectPlace learningen_HK
dc.subjectSynaptic plasticityen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAnxiety - geneticsen_HK
dc.subject.meshBehavior, Animal - physiologyen_HK
dc.subject.meshChimeraen_HK
dc.subject.meshElectrophysiologyen_HK
dc.subject.meshGene Targeting - methodsen_HK
dc.subject.meshHippocampus - cytology - physiologyen_HK
dc.subject.meshImmunohistochemistryen_HK
dc.subject.meshIntegrases - biosynthesis - geneticsen_HK
dc.subject.meshLearning - physiologyen_HK
dc.subject.meshLong-Term Potentiation - geneticsen_HK
dc.subject.meshMaleen_HK
dc.subject.meshMaze Learning - physiologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Inbred C57BLen_HK
dc.subject.meshMice, Mutant Strainsen_HK
dc.subject.meshMice, Transgenicen_HK
dc.subject.meshMotor Activity - geneticsen_HK
dc.subject.meshNeural Cell Adhesion Molecule L1 - deficiency - genetics - metabolismen_HK
dc.subject.meshNeuronal Plasticity - physiologyen_HK
dc.subject.meshProsencephalon - cytology - metabolismen_HK
dc.subject.meshSpatial Behavior - physiologyen_HK
dc.subject.meshSynaptic Transmission - geneticsen_HK
dc.subject.meshViral Proteins - biosynthesis - geneticsen_HK
dc.titleDecreased Anxiety, Altered Place Learning, and Increased CA1 Basal Excitatory Synaptic Transmission in Mice with Conditional Ablation of the Neural Cell Adhesion Molecule L1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-6474&volume=23&issue=32&spage=10419&epage=10432&date=2003&atitle=Decreased+anxiety,+altered+place+learning,+and+increased+CA1+basal+excitatory+synaptic+transmission+in+mice+with+conditional+ablation+of+the+neural+cell+adhesion+molecule+L1en_HK
dc.identifier.emailChung, SK:skchung@hkucc.hku.hken_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.pmid14614101-
dc.identifier.scopuseid_2-s2.0-0344393011en_HK
dc.identifier.hkuros91103-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0344393011&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume23en_HK
dc.identifier.issue32en_HK
dc.identifier.spage10419en_HK
dc.identifier.epage10432en_HK
dc.identifier.isiWOS:000186536100027-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLaw, JWS=7202548738en_HK
dc.identifier.scopusauthoridLee, AYW=8072063500en_HK
dc.identifier.scopusauthoridSun, M=7403180686en_HK
dc.identifier.scopusauthoridNikonenko, AG=7005667285en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridDityatev, A=13604932400en_HK
dc.identifier.scopusauthoridSchachner, M=7203055860en_HK
dc.identifier.scopusauthoridMorellini, F=6508006602en_HK

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