PMID- 28939187
OWN - NLM
STAT- MEDLINE
DCOM- 20180703
LR  - 20191210
IS  - 1878-4216 (Electronic)
IS  - 0278-5846 (Linking)
VI  - 81
DP  - 2018 Feb 2
TI  - The ameliorative effects and underlying mechanisms of dopamine D1-like receptor 
      agonist SKF38393 on Abeta(1-42)-induced cognitive impairment.
PG  - 250-261
LID - S0278-5846(17)30523-7 [pii]
LID - 10.1016/j.pnpbp.2017.09.017 [doi]
AB  - Alzheimer's disease (AD) is an age-related neurodegenerative disease 
      characterized by extracellular amyloid plaques and intracellular neurofibrillary 
      tangles. It is the most common form of human cognitive decline and dementia. In 
      this study, we aim to systematically investigate the ameliorative effects of 
      dopamine D1-like receptor agonist SKF38393 on cognitive dysfunction and explore 
      its underlying mechanisms. The Abeta(1-42) was injected intracerebroventricularly to 
      establish cognitive disorder model. Then, a series of behavior tests were used. 
      In order to further study the mechanisms, some relevant protein was assessed by 
      ELISA method and Western blot. The results in behavior tests revealed that 
      SKF38393 significantly ameliorated all the test indexes compared with the model 
      mice. Then SKF38393 increased phosphorylation of cAMP response element binding 
      protein (CREB) and expression of Bcl-2 in Western blot analyses. Furthermore, in 
      ELISA assay, SKF38393 significantly increased the brain-derived neurotrophic 
      factor (BDNF) levels and reduced the beta-site APP cleaving enzyme1 (BACE1) and 
      Abeta(1-42) levels in hippocampus and cortex of mice. However, compared with 
      SKF38393-H, all these results were significantly reversed by the dopamine D1 
      receptor antagonist SCH23390. These results indicated that SKF38393 could 
      ameliorate Abeta(1-42)-induced cognitive dysfunction in mice, which may be related 
      to D1 receptor activation. It leads to the phosphorylation of CREB, which promote 
      the expression of BDNF, Bcl-2 and decrease the expression of Abeta(1-42) of mice. 
      Our findings suggest that dopamine D1-like receptor may be a potential target for 
      the treatment of AD and its agonists may become a novel drug in the future.
CI  - Copyright (c) 2017 Elsevier Inc. All rights reserved.
FAU - Zang, Xuan
AU  - Zang X
AD  - Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, 
      China.
FAU - Cheng, Zhao-Yan
AU  - Cheng ZY
AD  - Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, 
      China.
FAU - Sun, Yi
AU  - Sun Y
AD  - Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, 
      China.
FAU - Hua, Nan
AU  - Hua N
AD  - Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, 
      China.
FAU - Zhu, Li-Hua
AU  - Zhu LH
AD  - Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, 
      China.
FAU - He, Ling
AU  - He L
AD  - Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, 
      China. Electronic address: heling@cpu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20170920
PL  - England
TA  - Prog Neuropsychopharmacol Biol Psychiatry
JT  - Progress in neuro-psychopharmacology & biological psychiatry
JID - 8211617
RN  - 0 (Amyloid beta-Peptides)
RN  - 0 (Benzazepines)
RN  - 0 (Dopamine Agonists)
RN  - 0 (Dopamine Antagonists)
RN  - 0 (Drd1 protein, mouse)
RN  - 0 (Nootropic Agents)
RN  - 0 (Peptide Fragments)
RN  - 0 (Receptors, Dopamine D1)
RN  - 0 (SCH 23390)
RN  - 0 (amyloid beta-protein (1-42))
RN  - 67287-49-4 (2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine)
RN  - EC 3.4.- (Amyloid Precursor Protein Secretases)
RN  - EC 3.4.23.- (Aspartic Acid Endopeptidases)
RN  - EC 3.4.23.46 (Bace1 protein, mouse)
SB  - IM
MH  - 2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-benzazepine/*pharmacology
MH  - Amyloid Precursor Protein Secretases/metabolism
MH  - Amyloid beta-Peptides/administration & dosage/*metabolism
MH  - Animals
MH  - Aspartic Acid Endopeptidases/metabolism
MH  - Benzazepines/pharmacology
MH  - Cerebral Cortex/drug effects/metabolism
MH  - Cognitive Dysfunction/*drug therapy/metabolism
MH  - Disease Models, Animal
MH  - Dopamine Agonists/*pharmacology
MH  - Dopamine Antagonists/pharmacology
MH  - Hippocampus/drug effects/metabolism
MH  - Learning/drug effects/physiology
MH  - Male
MH  - Memory/drug effects/physiology
MH  - Mice, Inbred ICR
MH  - Nootropic Agents/*pharmacology
MH  - Peptide Fragments/administration & dosage/*metabolism
MH  - Receptors, Dopamine D1/*agonists/antagonists & inhibitors/metabolism
OTO - NOTNLM
OT  - Alzheimer's disease
OT  - Behavioral test
OT  - Cognitive impairment
OT  - Dopamine D1-like receptor
OT  - cAMP response element binding protein
EDAT- 2017/09/25 06:00
MHDA- 2018/07/04 06:00
CRDT- 2017/09/24 06:00
PHST- 2017/06/30 00:00 [received]
PHST- 2017/08/30 00:00 [revised]
PHST- 2017/09/18 00:00 [accepted]
PHST- 2017/09/25 06:00 [pubmed]
PHST- 2018/07/04 06:00 [medline]
PHST- 2017/09/24 06:00 [entrez]
AID - S0278-5846(17)30523-7 [pii]
AID - 10.1016/j.pnpbp.2017.09.017 [doi]
PST - ppublish
SO  - Prog Neuropsychopharmacol Biol Psychiatry. 2018 Feb 2;81:250-261. doi: 
      10.1016/j.pnpbp.2017.09.017. Epub 2017 Sep 20.