TY - JOUR
T1 - A defect in nurturing in mice lacking the immediate early gene fosB
AU - Brown, Jennifer R.
AU - Ye, Hong
AU - Bronson, Roderick T.
AU - Dikkes, Pieter
AU - Greenberg, Michael E.
N1 - Funding Information:
We thank Arlene Sharpe for J1 embryonic stem cells and for advice on their proper handling, Steve Finkbeiner for photography of the mice, Nobuki Nakanishi for access to his water maze apparatus, Cliff Saper and Nancy Chamberlain for analysis of hypothalamic anatomy, Yusaku Nakabeppu for the anti-FosB N terminal antibody, Ron Wisdom for two anti-FosB antibodies, and A. F. Parlow and the National Hormone and Pituitary Program for rabbit anti-prolactin (mouse) antiserum (AFP 131078). We thank members of the Grenberg laboratory, particularly Seth Field, for helpful discussions and advice. This research was supported by the National Institutes of Health NIH RO1 Grant CA43855 to M. E. G., by MRRC Grant NIH P30-HD18655, and by an American Cancer Society Faculty Research Award (FRA-379) to M. E. G.
PY - 1996/7/26
Y1 - 1996/7/26
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=0030602817&partnerID=8YFLogxK
U2 - 10.1016/S0092-8674(00)80101-4
DO - 10.1016/S0092-8674(00)80101-4
M3 - Article
C2 - 8706134
AN - SCOPUS:0030602817
SN - 0092-8674
VL - 86
SP - 297
EP - 309
JO - Cell
JF - Cell
IS - 2
ER -