A defect in nurturing in mice lacking the immediate early gene fosB

被引:259
作者
Brown, JR
Ye, H
Bronson, RT
Dikkes, P
Greenberg, ME
机构
[1] HARVARD UNIV, SCH MED, DEPT NEUROBIOL, BOSTON, MA 02115 USA
[2] TUFTS UNIV, SCH VET MED, SCH MED, DEPT PATHOL, BOSTON, MA 02111 USA
关键词
D O I
10.1016/S0092-8674(00)80101-4
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Although expression of the Fos family of transcription factors is induced by environmental stimuli that trigger adaptive neuronal responses, evidence that Fos family members mediate these responses is lacking. To address this issue, mice were generated with an inactivating mutation in the fosB gene. fosB mutant mice are profoundly deficient in their ability to nurture young animals but are normal with respect to other cognitive and sensory functions. The nurturing defect is likely due to the absence of FosB in the preoptic area, a region of the hypothalamus that is critical for nurturing. These observations suggest that a transcription factor controls a complex behavior by regulating a specific neuronal circuit and indicate that nurturing in mammals has a genetic component.
引用
收藏
页码:297 / 309
页数:13
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