PMID- 28594546
OWN - NLM
STAT- MEDLINE
DCOM- 20180612
LR  - 20191210
IS  - 1948-7193 (Electronic)
IS  - 1948-7193 (Linking)
VI  - 8
IP  - 9
DP  - 2017 Sep 20
TI  - Neuropeptide VGF C-Terminal Peptide TLQP-62 Alleviates Lipopolysaccharide-Induced 
      Memory Deficits and Anxiety-like and Depression-like Behaviors in Mice: The Role 
      of BDNF/TrkB Signaling.
PG  - 2005-2018
LID - 10.1021/acschemneuro.7b00154 [doi]
AB  - Peripheral inflammatory responses affect central nervous system (CNS) function, 
      manifesting in symptoms of memory deficits, depression, and anxiety. Previous 
      studies have revealed that neuropeptide VGF (nonacronymic) C-terminal peptide 
      TLQP-62 rapidly reinforces brain-derived neurotrophic factor (BDNF)/tropomyosin 
      receptor kinase B (TrkB) signaling, regulating memory consolidation and 
      antidepressant-like action. However, whether it is beneficial for 
      lipopolysaccharide (LPS)-induced neuropsychiatric dysfunction in mice is unknown. 
      Herein, we explored the involvement of BDNF/TrkB signaling and biochemical 
      alterations in inflammatory or oxidative stress markers in the alleviating 
      effects of TLQP-62 on LPS-induced neuropsychiatric dysfunction. The mice were 
      treated with TLQP-62 (2 mug/side) via intracerebroventricular (i.c.v.) injection 1 
      h before LPS (0.5 mg/kg, i.p.) administration. Our results showed that a single 
      treatment with LPS (0.5 mg/kg, i.p) is sufficient to produce recognition memory 
      deficits (in the novel object recognition test), depression-like behavior (in the 
      forced swim test and sucrose preference test), and anxiety-like behavior (in the 
      elevated zero maze). However, pretreatment with TLQP-62 prevented LPS-induced 
      behavioral dysfunction, neuroinflammatory, and oxidative responses. In addition, 
      our results further demonstrated that a reduction in BDNF expression mediated by 
      BDNF-shRNA lentivirus significantly blocked the effects of TLQP-62, suggesting 
      the critical role of BDNF/TrkB signaling in the neuroprotective effects of 
      TLQP-62 in the mice. In conclusion, TLQP-62 could be a therapeutic approach for 
      neuropsychiatric disorders, which are closely associated with neuroinflammation 
      and oxidative stress.
FAU - Li, Chenli
AU  - Li C
FAU - Li, Mengmeng
AU  - Li M
FAU - Yu, Hanjie
AU  - Yu H
FAU - Shen, Xinbei
AU  - Shen X
FAU - Wang, Jinting
AU  - Wang J
FAU - Sun, Xin
AU  - Sun X
FAU - Wang, Qinwen
AU  - Wang Q
FAU - Wang, Chuang
AU  - Wang C
AUID- ORCID: 0000-0002-3816-230X
AD  - Li Dak Sum Yip Yio Chin Kenneth Li Marine Biopharmaceutical Research Center, 
      Ningbo University , Ningbo 315211, China.
LA  - eng
PT  - Journal Article
DEP - 20170621
PL  - United States
TA  - ACS Chem Neurosci
JT  - ACS chemical neuroscience
JID - 101525337
RN  - 0 (Anti-Anxiety Agents)
RN  - 0 (Anti-Inflammatory Agents)
RN  - 0 (Antidepressive Agents)
RN  - 0 (Brain-Derived Neurotrophic Factor)
RN  - 0 (Lipopolysaccharides)
RN  - 0 (Nootropic Agents)
RN  - 0 (Peptides)
RN  - 0 (TLQP62 peptide)
RN  - EC 2.7.10.1 (Receptor, trkB)
SB  - IM
MH  - Animals
MH  - Anti-Anxiety Agents/*pharmacology
MH  - Anti-Inflammatory Agents/*pharmacology
MH  - Antidepressive Agents/*pharmacology
MH  - Anxiety/drug therapy/immunology
MH  - Brain/drug effects/immunology
MH  - Brain-Derived Neurotrophic Factor/metabolism
MH  - Depressive Disorder/drug therapy/immunology
MH  - Disease Models, Animal
MH  - Escherichia coli
MH  - Lipopolysaccharides
MH  - Male
MH  - Memory Disorders/drug therapy/immunology
MH  - Mice, Inbred ICR
MH  - Motor Activity/drug effects/physiology
MH  - Nootropic Agents/*pharmacology
MH  - Oxidative Stress/drug effects/physiology
MH  - Peptides/*pharmacology
MH  - Receptor, trkB/metabolism
MH  - Recognition, Psychology/drug effects/physiology
MH  - Signal Transduction/drug effects
OTO - NOTNLM
OT  - TLQP-62
OT  - brain-derived neurotrophic factor
OT  - lipopolysaccharide
OT  - neuroinflammation
OT  - neuropsychiatric dysfunction
OT  - oxidative stress
EDAT- 2017/06/09 06:00
MHDA- 2018/06/13 06:00
CRDT- 2017/06/09 06:00
PHST- 2017/06/09 06:00 [pubmed]
PHST- 2018/06/13 06:00 [medline]
PHST- 2017/06/09 06:00 [entrez]
AID - 10.1021/acschemneuro.7b00154 [doi]
PST - ppublish
SO  - ACS Chem Neurosci. 2017 Sep 20;8(9):2005-2018. doi: 10.1021/acschemneuro.7b00154. 
      Epub 2017 Jun 21.