NCAM deficiency in the mouse forebrain impairs innate and learned avoidance behaviours

J. Brandewiede, O. Stork, Melitta Camartin

Research output: Contribution to journalArticlepeer-review

7 Scopus citations

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 nullmutants 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 mutantswas 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.

Original languageEnglish (US)
Pages (from-to)468-477
Number of pages10
JournalGenes, Brain and Behavior
Volume13
Issue number5
DOIs
StatePublished - 2014

All Science Journal Classification (ASJC) codes

  • Genetics
  • Neurology
  • Behavioral Neuroscience

Keywords

  • Aggression
  • Amygdala
  • Anxiety
  • Conditional knockout
  • Hippocampus
  • Mouse
  • NCAM
  • Passive avoidance
  • Serotonin
  • Stress

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