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Date: 15 December 2011

Journal: Journal of Neuroimmunology Volume 240-241, 15 December 2011, Pages 45-51 , Doi: 10.1016/j.jneuroim.2011.09.008

2011 | T-bet deficient mice exhibit resistance to stress-induced development of depression-like behaviors…

Kim, S.-J.a, Lee, H.a, Joung, H.-Y.b, Lee, G.a, Lee, H.-J.a, Shin, M.-K.a, Kim, S.-H.c, Shim, I.b, Bae, H.a

Abstract

T-bet, a Th1-specific T-box transcription factor, regulates Th1 development by inducing endogenous Th1 cytokines and IFN-γ. This study was conducted to determine if T-bet knockout mice exhibit resistance to stress-induced development of depression-like behaviors. The T-bet knockout mice significantly reduced depressive-like behaviors provoked by repeated restraint stress in an elevated plus-maze test (EPM), tail suspension test (TST), and forced swim test (FST). Moreover, stress-induced elevations of the pro-inflammatory cytokines were attenuated in T-bet deficient group. These results suggest that T-bet directly mediated stress-induced depression. Therefore, understanding T-bet function during stress represents an additional treatment strategy for depression. © 2011 Elsevier B.V.


Author keywords

Behavior; Cytokine; Depression; Monoamine; T-bet


Indexed keywords

EMTREE drug terms: cytokine; transcription factor T bet

EMTREE medical terms: animal experiment; article; controlled study; depression; disease resistance; elevated plus maze test; experimental test; forced swimming test; gene silencing; immobilization stress; male; maze test; mouse; nonhuman; priority journal; protein function; stress; tail suspension test

MeSH: Animals; Anxiety; Cytokines; Depression; Hindlimb Suspension; Inflammation Mediators; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Random Allocation; Restraint, Physical; Stress, Physiological; T-Box Domain Proteins
Medline is the source for the MeSH terms of this document.


Chemicals and CAS Registry Numbers: Cytokines; Inflammation Mediators; T-Box Domain Proteins; T-box transcription factor TBX21


ISSN: 01655728 CODEN: JNRIDSource Type: Journal Original language: English
DOI: 10.1016/j.jneuroim.2011.09.008 PubMed ID: 22018704 Document Type: Article
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