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Publication : The influence of a targeted deletion of the IFNgamma gene on emotional behaviors.

First Author  Kustova Y Year  1998
Journal  Brain Behav Immun Volume  12
Issue  4 Pages  308-24
PubMed ID  10080860 Mgi Jnum  J:54250
Mgi Id  MGI:1334851 Doi  10.1006/brbi.1998.0546
Citation  Kustova Y, et al. (1998) The influence of a targeted deletion of the IFNgamma gene on emotional behaviors. Brain Behav Immun 12(4):308-24
abstractText  Evidence suggests that interferon-gamma (IFNgamma) plays an important role in CNS function and development. While the paucity of agents that selectively modify IFNgamma production or interaction with its receptors makes analyses of its potential behavioral relevance difficult, mice with null mutations of the IFNgamma gene have been used to investigate the potential role of IFNgamma in emotional behaviors. C57Bl/6 (B6) mice with null mutations of the IFNgamma gene (IFNgamma (-/-)) showed significantly increased emotionality compared to the wild-type (IFNgamma (+/+)) B6 mice. This was manifested in performance in the elevated plus maze as well as increased defecation scores and decreased locomotor activity both in novel environments and following a sonic stimulus. In contrast, the general level of emotionality of both IFNgamma (+/+) and (-/-) BALB/c (C) mice was substantially greater than that of either of the B6 mouse groups. While C IFNgamma (-/-) showed increased immobility in response to novelty, other indices of emotionality of C IFNgamma (-/-) mice were not significantly different from those of the C IFNgamma (+/+) mice. In summary, the lack of IFNgamma appears to contribute to increased emotionality, but the basal behaviors of the parental strain (e.g., BALBc) may overshadow the expression of this emotionality. While mice with null mutations of the IFNgamma gene may be useful tools for investigating the role of IFNgamma in brain function and behavior, the influence of the parent strain genome(s) on the behaviors in question must be taken into account. Copyright 1998 Academic Press.
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