| First Author | Kuroda KO | Year | 2008 |
| Journal | Brain Res | Volume | 1211 |
| Pages | 57-71 | PubMed ID | 18423429 |
| Mgi Jnum | J:136816 | Mgi Id | MGI:3797162 |
| Doi | 10.1016/j.brainres.2008.02.100 | Citation | Kuroda KO, et al. (2008) Neurobehavioral basis of the impaired nurturing in mice lacking the immediate early gene FosB. Brain Res 1211:57-71 |
| abstractText | The transcription factor FosB is induced in neurons of the medial preoptic area (MPOA) during parenting, through activation of the extracellular signal-regulated kinase (ERK). FosB mutant (-/-) postpartum mice and virgin mice that are exposed to pups show defective nurturing behavior. The FosB (-/-) MPOA fails to fully up-regulate SPRY1 and Rad, the feedback regulators of ERK and calcium signaling, respectively. Here we studied FosB function by examining the gene expression profiles and the behavioral characteristics of FosB (-/-) mice. We found that FosB (-/|-) mice exhibited not only decreased parenting but also decreased infanticide compared with (+/) littermates. We then performed gene expression analysis in the MPOA of FosB (-/-) mice compared with the wild-type littermates. We found up-regulation of glial fibrillary acidic protein (GFAP), C4, and Ela1 mRNA in the MPOA of FosB (-/-) mice; all of these gene products were implicated in general neuropathological conditions. Immunohistochemical analysis showed that up-regulation of GFAP was not restricted to MPOA but extended throughout the forebrain, including the cerebral cortex and striatum. Such pervasive GFAP up-regulation suggested that FosB (-/-) mice might have other behavioral abnormalities than nurturing. Indeed, these mice showed a clear alteration in emotionality, detected by the acoustic startle, elevated plus maze, and passive avoidance tests. These results suggest that FosB (-/-) mice have broader neurobehavioral dysfunctions, with which the nurturing defect might share the common mechanism. |
