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Brain Behav Immun. 2019 Jan 22. pii: S0889-1591(18)30632-9. doi: 10.1016/j.bbi.2019.01.022. [Epub ahead of print]

Transplantation with mGluR5 deficiency bone marrow displays antidepressant-like effect in C57BL/6J mice.

Author information

1
Department of Biochemistry and Molecular Biology, Army Medical University, Chongqing 400038, PR China.
2
Department of Neurosurgery, Daping Hospital, Army Medical University, Chongqing 400042, PR China.
3
Molecular Biology Center, State Key Laboratory of Trauma, Burn, and Combined Injury, Daping Hospital, Army Medical University, Chongqing 400042, PR China.
4
Department of Biochemistry and Molecular Biology, Army Medical University, Chongqing 400038, PR China; Molecular Biology Center, State Key Laboratory of Trauma, Burn, and Combined Injury, Daping Hospital, Army Medical University, Chongqing 400042, PR China. Electronic address: tmmubiodss66@aliyun.com.

Abstract

Antidepressant-like effects of metabotropic glutamate receptor 5 (mGluR5) have been verified by specific antagonists or whole body knock-out (KO) mice. Previous experiments indicate that blocking mGluR5 exerts antidepressant-like effects through neuronal mechanisms, like modulating NMDA receptor activity or 5-HT system. Here we found that transplanting bone marrow from mGluR5 KO mice to WT mice could also show antidepressant-like effects, which were confirmed by sucrose preference test and tail suspension test. Furthermore, mGluR5 deficiency dramatically inhibits cytokines release from bone marrow cells, such as IL-1β, TNF-α and IL-6, alleviating proinflammatory responses in LPS-induced depression model. In addition, inhibited cytokines could decrease the activation of brain endothelial cells in ERK-dependent manner. These data provide the evidence that blocking mGluR5 could improve depression through inhibiting peripheral immune responses, confirming the causal relationship between peripheral immune phenotype and brain behavior.

KEYWORDS:

Bone marrow transplantation; Depression; LPS; mGluR5

PMID:
30682501
DOI:
10.1016/j.bbi.2019.01.022

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