Journal
CELL
Volume 173, Issue 5, Pages 1265-+Publisher
CELL PRESS
DOI: 10.1016/j.cell.2018.03.037
Keywords
-
Categories
Funding
- National Institutes Health [MH085082, MH112593, MH070053]
- Gordon Moore Foundation [2646]
- Ellison Medical Research Foundation [NR-AA-0108-12]
- Simons Foundation
- NARSAD Young Investigator Award [23687]
- L'OREAL for Women in Science award
- NIMH K99 Pathway to Independence Award [MH108734]
Ask authors/readers for more resources
Chronic social isolation causes severe psychological effects in humans, but their neural bases remain poorly understood. 2 weeks (but not 24 hr) of social isolation stress (SIS) caused multiple behavioral changes in mice and induced brain-wide upregulation of the neuropeptide tachykinin 2 (Tac2)/neurokinin B (NkB). Systemic administration of an Nk3R antagonist prevented virtually all of the behavioral effects of chronic SIS. Conversely, enhancing NkB expression and release phenocopied SIS in group-housed mice, promoting aggression and converting stimulus-locked defensive behaviors to persistent responses. Multiplexed analysis of Tac2/NkB function in multiple brain areas revealed dissociable, region-specific requirements for both the peptide and its receptor in different SIS-induced behavioral changes. Thus, Tac2 coordinates a pleiotropic brain state caused by SIS via a distributed mode of action. These data reveal the profound effects of prolonged social isolation on brain chemistry and function and suggest potential new therapeutic applications for Nk3R antagonists.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available