PMID- 29390063
OWN - NLM
STAT- MEDLINE
DCOM- 20190501
LR  - 20190501
IS  - 1469-5111 (Electronic)
IS  - 1461-1457 (Print)
IS  - 1461-1457 (Linking)
VI  - 21
IP  - 5
DP  - 2018 May 1
TI  - The Dopamine Receptor D3 Regulates Lipopolysaccharide-Induced Depressive-Like 
      Behavior in Mice.
PG  - 448-460
LID - 10.1093/ijnp/pyy005 [doi]
AB  - BACKGROUND: The altered expression and function of dopamine receptor D3 (D3R) in 
      patients and animal models have been correlated with depression disease severity. 
      However, the morphological alterations and biological effects of D3R in the brain 
      after inflammation-induced depressive-like behavior remain elusive. METHODS: In 
      the present study, we ascertained the changes of D3R expression in the brain 
      regions after depressive-like behavior induced by peripheral administration of 
      lipopolysaccharide (LPS). Protein levels of proinflammatory cytokines, 
      brain-derived neurotrophic factor (BDNF), and extracellular signal-regulated 
      kinase (ERK1/2)-cAMP-response element-binding protein (CREB) signaling pathway 
      after activation or inhibition of D3R in the brain of depressive mice were also 
      investigated. RESULTS: LPS caused a significant reduction of D3R in the ventral 
      tegmental area (VTA), medial prefrontal cortex (mPFC), and nucleus accumbens 
      (NAc), which are areas related to the mesolimbic dopaminergic system. 
      Pretreatment with pramipexole (PPX), a preferential D3R agonist, showed 
      antidepressant effects on LPS-induced depression-like behavior through preventing 
      changes in LPS-induced proinflammatory cytokines (tumour necrosis factor-alpha, 
      interleukin-1beta, and interleukin-6), BDNF, and ERK1/2-CREB signaling pathway in 
      the VTA and NAc. In opposition, treatment with a D3R selective antagonist NGB 
      2904 alone made mice susceptible to depression-like effects and caused changes in 
      accordance with the LPS-induced alterations in proinflammatory cytokines, BDNF, 
      and the ERK1/2-CREB signaling pathway in the mPFC and NAc. CONCLUSIONS: These 
      findings provide a relevant mechanism for D3R in LPS-induced depressive-like 
      behavior via its mediation of proinflammatory cytokines and potential 
      cross-effects between BDNF and the ERK1/2-CREB signaling pathway.
FAU - Wang, Jing
AU  - Wang J
AD  - Department of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an 
      Jiaotong University Health Science Center, Xi'an, China.
FAU - Jia, Yuwei
AU  - Jia Y
AD  - Department of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an 
      Jiaotong University Health Science Center, Xi'an, China.
FAU - Li, Guodong
AU  - Li G
AD  - Department of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an 
      Jiaotong University Health Science Center, Xi'an, China.
FAU - Wang, Biao
AU  - Wang B
AD  - Department of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an 
      Jiaotong University Health Science Center, Xi'an, China.
FAU - Zhou, Ting
AU  - Zhou T
AD  - Department of Laboratory Medicine, The Second Affiliated Hospital, Xi'an Jiaotong 
      University Health Science Center, Xi'an, China.
FAU - Zhu, Li
AU  - Zhu L
AD  - Forensic Medicine College of Xi'an Jiaotong University, Key Laboratory of the 
      Health Ministry for Forensic Medicine, Xi'an, China.
FAU - Chen, Teng
AU  - Chen T
AD  - Forensic Medicine College of Xi'an Jiaotong University, Key Laboratory of the 
      Health Ministry for Forensic Medicine, Xi'an, China.
FAU - Chen, Yanjiong
AU  - Chen Y
AD  - Department of Immunology and Pathogenic Biology, College of Basic Medicine, Xi'an 
      Jiaotong University Health Science Center, Xi'an, China.
AD  - Forensic Medicine College of Xi'an Jiaotong University, Key Laboratory of the 
      Health Ministry for Forensic Medicine, Xi'an, China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Int J Neuropsychopharmacol
JT  - The international journal of neuropsychopharmacology
JID - 9815893
RN  - 0 (Dopamine Agonists)
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Drd3 protein, mouse)
RN  - 0 (Fluorenes)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (NGB 2904)
RN  - 0 (Piperazines)
RN  - 0 (Receptors, Dopamine D3)
RN  - 83619PEU5T (Pramipexole)
SB  - IM
MH  - Animals
MH  - Behavior, Animal/drug effects/*physiology
MH  - Brain/drug effects/*metabolism
MH  - *Depression/chemically induced/immunology/metabolism/physiopathology
MH  - Disease Models, Animal
MH  - Dopamine Agonists/administration & dosage/*pharmacology
MH  - Dopamine Antagonists/administration & dosage/*pharmacology
MH  - Fluorenes/pharmacology
MH  - Lipopolysaccharides/administration & dosage/*pharmacology
MH  - Male
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Nucleus Accumbens/drug effects/metabolism
MH  - Piperazines/pharmacology
MH  - Pramipexole/pharmacology
MH  - Prefrontal Cortex/drug effects/metabolism
MH  - Receptors, Dopamine D3/drug effects/*metabolism
MH  - Signal Transduction/drug effects/*physiology
MH  - Ventral Tegmental Area/drug effects/metabolism
PMC - PMC5932470
EDAT- 2018/02/02 06:00
MHDA- 2019/05/02 06:00
PMCR- 2018/01/30
CRDT- 2018/02/02 06:00
PHST- 2017/09/14 00:00 [received]
PHST- 2018/01/26 00:00 [accepted]
PHST- 2018/02/02 06:00 [pubmed]
PHST- 2019/05/02 06:00 [medline]
PHST- 2018/02/02 06:00 [entrez]
PHST- 2018/01/30 00:00 [pmc-release]
AID - 4829760 [pii]
AID - pyy005 [pii]
AID - 10.1093/ijnp/pyy005 [doi]
PST - ppublish
SO  - Int J Neuropsychopharmacol. 2018 May 1;21(5):448-460. doi: 10.1093/ijnp/pyy005.