PMID- 30753874
OWN - NLM
STAT- MEDLINE
DCOM- 20200309
LR  - 20200309
IS  - 1872-7549 (Electronic)
IS  - 0166-4328 (Linking)
VI  - 364
DP  - 2019 May 17
TI  - Neuronostatin promotes soluble Abeta1-42 oligomers -induced spatial learning and 
      memory impairments in mice.
PG  - 62-74
LID - S0166-4328(18)31588-2 [pii]
LID - 10.1016/j.bbr.2019.01.047 [doi]
AB  - Neuronostatin (NST) is composed of a 13-amino acid and amidated peptide hormone 
      encoded in the somatostatin (SST) gene, and plays an important physiological 
      function in diverse tissues. Previous studies have shown that 
      intracerebroventricular (i.c.v.) and intra-hippocampally administration of NST 
      can significantly decrease the percentage of novel object exploration time in the 
      step-down test. In this study, to define the contribution of NST to cognitive 
      impairments induced by soluble Abeta42 oligomers (oAbeta), along with the underlying 
      mechanisms. This study used behavioral, biochemical and immunohistological 
      methods to find that i.c.v. administration of NST (3 nmol/mouse) disrupted the 
      ability of spatial learning and memory in mice, led to increase the levels of 
      cAMP, GPR107 protein expression and phosphorylation of PKA at Thr197 in the 
      cortex and hippocampus. NST promoted oAbeta (1 nmol/mouse) -induced cognitive 
      impairments, subsequently co-injection of NST and oAbeta increased the levels of 
      GPR107 expression and PKA phosphorylation, which also led to hyperactivation of 
      GFAP in the cortex and neuroinflammation cytokines (IL-1beta, IL-6 and TNFalpha) both in 
      the cortex and hippocampus. Moreover, it was demonstrated that co-administration 
      of NST and oAbeta had increased the phosphorylation of Akt and GSK3beta and reduced the 
      levels of ATP and hexokinase (HK) activity in the cortex. Therefore, taken 
      together, this study provided powerful insight into the mechanism of NST for 
      memory impairments induced by oAbeta, and may potentially serve as a promising 
      target for future Alzheimer's disease interventions.
CI  - Copyright (c) 2019 Elsevier B.V. All rights reserved.
FAU - Yang, Shaobin
AU  - Yang S
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China. Electronic address: shaobin.yang5@gmail.com.
FAU - Shao, Tingji
AU  - Shao T
AD  - Department of Pharmacy, Gansu Provincial People's Hospital, Lanzhou, Gansu, 
      730000, China.
FAU - Yu, Peng
AU  - Yu P
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China.
FAU - Cao, Ruidong
AU  - Cao R
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China.
FAU - Zhang, Mingyu
AU  - Zhang M
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China.
FAU - Wen, Kang
AU  - Wen K
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China.
FAU - Fan, Maorong
AU  - Fan M
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China.
FAU - He, Bosheng
AU  - He B
AD  - College of Life Sciences, Northwest Normal University, Lanzhou, Gansu, 730070, 
      China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20190210
PL  - Netherlands
TA  - Behav Brain Res
JT  - Behavioural brain research
JID - 8004872
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (GPR107 protein, mouse)
RN  - 0 (Neuroprotective Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (Peptide Hormones)
RN  - 0 (Receptors, G-Protein-Coupled)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (neuronostatin, mouse)
RN  - 51110-01-1 (Somatostatin)
SB  - IM
MH  - Alzheimer Disease/metabolism
MH  - Amyloid beta-Peptides/adverse effects/metabolism
MH  - Animals
MH  - Cognition/drug effects
MH  - Cognitive Dysfunction/metabolism
MH  - Disease Models, Animal
MH  - Hippocampus/metabolism
MH  - Male
MH  - Maze Learning/drug effects
MH  - Memory/*drug effects
MH  - Memory Disorders/chemically induced
MH  - Mice
MH  - Neuroprotective Agents/pharmacology
MH  - Peptide Fragments/pharmacology
MH  - Peptide Hormones/*metabolism/pharmacology/physiology
MH  - Receptors, G-Protein-Coupled/metabolism
MH  - Somatostatin/metabolism
MH  - Spatial Learning/*drug effects
MH  - Tumor Necrosis Factor-alpha/metabolism
OTO - NOTNLM
OT  - Abeta1-42
OT  - G-protein-coupled receptor 107
OT  - Glucose
OT  - Inflammation
OT  - Memory
OT  - Neuronostatin
EDAT- 2019/02/13 06:00
MHDA- 2020/03/10 06:00
CRDT- 2019/02/13 06:00
PHST- 2018/11/10 00:00 [received]
PHST- 2019/01/06 00:00 [revised]
PHST- 2019/01/25 00:00 [accepted]
PHST- 2019/02/13 06:00 [pubmed]
PHST- 2020/03/10 06:00 [medline]
PHST- 2019/02/13 06:00 [entrez]
AID - S0166-4328(18)31588-2 [pii]
AID - 10.1016/j.bbr.2019.01.047 [doi]
PST - ppublish
SO  - Behav Brain Res. 2019 May 17;364:62-74. doi: 10.1016/j.bbr.2019.01.047. Epub 2019 
      Feb 10.