title: NCAM deficiency in the mouse forebrain impairs innate and learned avoidance behaviours.
abstract: The neural cell adhesion molecule (NCAM) has been implicated in the development and plasticity of neural circuits and the control of hippocampus- and amygdala-dependent learning and behaviour. Previous studies in constitutive NCAM null mutants identified emotional behaviour deficits related to disturbances of hippocampal and amygdala functions. Here, we studied these behaviours in mice conditionally deficient in NCAM in the postmigratory forebrain neurons. We report deficits in both innate and learned avoidance behaviours, as observed in elevated plus maze and passive avoidance tasks. In contrast, general locomotor activity, trait anxiety or neophobia were unaffected by the mutation. Altered avoidance behaviour of the conditional NCAM mutants was associated with a deficit in serotonergic signalling, as indicated by their reduced responsiveness to (±)-8-hydroxy-2-(dipropylamino)-tetralin-induced hypothermia. Another serotonin-dependent behaviour, namely intermale aggression that is massively increased in constitutively NCAM-deficient mice, was not affected in the forebrain-specific mutants. Our data suggest that genetically or environmentally induced changes of NCAM expression in the late postnatal and mature forebrain determine avoidance behaviour and serotonin (5-HT)1A receptor signalling.
authors.affiliation: Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Universität Hamburg, Hamburg.
authors.forename: J
authors.initials: J
authors.lastname: Brandewiede
authors.affiliation: Department of Genetics and Molecular Neurobiology, Institute of Biology, Otto-von-Guericke University.|Center for Behavioural Brain Sciences, Magdeburg, Germany.
authors.forename: O
authors.initials: O
authors.lastname: Stork
authors.affiliation: Zentrum für Molekulare Neurobiologie Hamburg, Universitätsklinikum Hamburg-Eppendorf, Universität Hamburg, Hamburg.|Keck Center for Collaborative Neuroscience and Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA.|Center for Neuroscience, Shantou University Medical College, Shantou, China.
authors.forename: M
authors.initials: M
authors.lastname: Schachner
mesh_terms: D000374:Aggression; D000818:Animals; D001362:Avoidance Learning; D018491:Dopamine Agonists / Q000494:pharmacology; D008297:Male; D018782:Maze Learning; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation; D019006:Neural Cell Adhesion Molecules / Q000172:deficiency / Q000235:genetics* / Q000378:metabolism; D016548:Prosencephalon / Q000187:drug effects / Q000378:metabolism* / Q000502:physiology
chemical_list: D018491:Dopamine Agonists; D019006:Neural Cell Adhesion Molecules
keywords: 5-HT1A; NCAM; aggression; amygdala; anxiety; conditional knockout; hippocampus; mouse; passive avoidance; serotonin; stress