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dc.contributor.authorTekinay, A.B.en_US
dc.contributor.authorNong, Y.en_US
dc.contributor.authorMiwa J.M.en_US
dc.contributor.authorLieberam I.en_US
dc.contributor.authorIbanez-Tallon I.en_US
dc.contributor.authorGreengard P.en_US
dc.contributor.authorHeintz, N.en_US
dc.date.accessioned2016-02-08T10:04:54Z
dc.date.available2016-02-08T10:04:54Z
dc.date.issued2009en_US
dc.identifier.issn0027-8424
dc.identifier.urihttp://hdl.handle.net/11693/22803
dc.description.abstractAnxiety disorders are the most prevalent mental disorders in developed societies. Although roles for the prefrontal cortex, amygdala, hippocampus and mediodorsal thalamus in anxiety disorders are well documented, molecular mechanisms contributing to the functions of these structures are poorly understood. Here we report that deletion of Lynx2, a mammalian prototoxin gene that is expressed at high levels in anxiety associated brain areas, results in elevated anxiety-like behaviors. We show that LYNX2 can bind to and modulate neuronal nicotinic receptors, and that loss of Lynx2 alters the actions of nicotine on glutamatergic signaling in the prefrontal cortex. Our data identify Lynx2 as an important component of the molecular mechanisms that control anxiety, and suggest that altered glutamatergic signaling in the prefrontal cortex of Lynx2 mutant mice contributes to increased anxiety-related behaviors.en_US
dc.language.isoEnglishen_US
dc.source.titleProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.relation.isversionofhttp://dx.doi.org/10.1073/pnas.0813109106en_US
dc.subjectAnxietyen_US
dc.subjectLYNX2en_US
dc.subjectNicotinicen_US
dc.subjectPrefrontal cortexen_US
dc.subjectglutamic aciden_US
dc.subjectlynx2 proteinen_US
dc.subjectnicotineen_US
dc.subjectnicotinic receptoren_US
dc.subjectproteinen_US
dc.subjectunclassified drugen_US
dc.subjectamygdaloid nucleusen_US
dc.subjectanimal experimenten_US
dc.subjectanimal tissueen_US
dc.subjectanxiety disorderen_US
dc.subjectarticleen_US
dc.subjectcontrolled studyen_US
dc.subjectdisease associationen_US
dc.subjectgeneen_US
dc.subjectgene deletionen_US
dc.subjectgene expressionen_US
dc.subjectgene functionen_US
dc.subjectgene lossen_US
dc.subjecthippocampusen_US
dc.subjecthumanen_US
dc.subjecthuman cellen_US
dc.subjectlynx2 geneen_US
dc.subjectmolecular mechanicsen_US
dc.subjectmouseen_US
dc.subjectneurotransmissionen_US
dc.subjectnonhumanen_US
dc.subjectprefrontal cortexen_US
dc.subjectpriority journalen_US
dc.subjectprotein localizationen_US
dc.subjectprotein protein interactionen_US
dc.subjectreceptor bindingen_US
dc.subjectregulator geneen_US
dc.subjectthalamus dorsomedial nucleusen_US
dc.subjectAnimalsen_US
dc.subjectAnxietyen_US
dc.subjectAnxiety Disordersen_US
dc.subjectBehavior, Animalen_US
dc.subjectGlutamic Aciden_US
dc.subjectMembrane Glycoproteinsen_US
dc.subjectMiceen_US
dc.subjectMice, Mutant Strainsen_US
dc.subjectNeuropeptidesen_US
dc.subjectProtein Bindingen_US
dc.subjectReceptors, Nicotinicen_US
dc.subjectSynaptic Transmissionen_US
dc.subjectMammaliaen_US
dc.subjectMusen_US
dc.titleA role for LYNX2 in anxiety-related behavioren_US
dc.typeArticleen_US
dc.departmentInstitute of Materials Science and Nanotechnology (UNAM)en_US
dc.citation.spage4477en_US
dc.citation.epage4482en_US
dc.citation.volumeNumber106en_US
dc.citation.issueNumber11en_US
dc.identifier.doi10.1073/pnas.0813109106en_US


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