PMID- 29804362
OWN - NLM
STAT- MEDLINE
DCOM- 20190329
LR  - 20220330
IS  - 1007-3418 (Print)
IS  - 1007-3418 (Linking)
VI  - 26
IP  - 1
DP  - 2018 Jan 20
TI  - [Effect of dopamine on intracerebral glutamate uptake ability in rats with 
      minimal hepatic encephalopathy and the pathogenesis of minimal hepatic 
      encephalopathy].
PG  - 48-53
LID - 10.3760/cma.j.issn.1007-3418.2018.01.011 [doi]
AB  - Objective: To investigate the effect of dopamine (DA) on the glutamate (Glu) 
      uptake ability of neural cells, as well as its effect on cognitive impairment in 
      rats with minimal hepatic encephalopathy (MHE) via related pathways. Methods: A 
      total of 45 Sprague-Dawley rats were randomly divided into control group, MHE 
      model group, and DA intervention model group, with 15 rats in each group. The 
      rats in the MHE model group were given intraperitoneal injection of thioacetamide 
      (TAA), those in DA intervention model group were given intraventricular injection 
      of DA, and those in the control group were given intraperitoneal injection of 
      physiological saline, with a frequency of twice a week for 8 weeks. Cerebral 
      microdialysis was used to measure the change in the content of Glu in the brain 
      in MHE rats and rats with DA intervention; RT-PCR and Western blotting were used 
      to measure the relative mRNA and protein expression of trace amine-associated 
      receptor 1 (TAAR1) and excitatory amino acid transporter 2 (EAAT2); the changes 
      in the expression of EAAT2 and extracellular Glu level were measured after 
      intracerebroventricular injection of TAAR1 siRNA and TAAR1 plasmid in MHE rats 
      and rats with DA intervention. One- way analyses of variance for comparison among 
      different groups were performed, categorical data between groups were compared 
      using nonparametric tests. Results: Compared with the control group, the MHE 
      model group had significant increases in the content of DA in liver tissue, 
      plasma, and brain tissue (4.90 +/- 0.13 ng/g vs 1.20 +/- 0.13 ng/g, P < 0.05; 16.32 +/- 
      1.01 pmol/ml vs 5.50 +/- 0.82 pmol/ml, P < 0.05; 732.45 +/- 78.85 ng/g vs 387.00 +/- 
      23.36 ng/g, P < 0.05). There was a significant increase in the extracellular Glu 
      level within 40-120 minutes after intracerebral injection of DA in the DA 
      intervention model group. Compared with the control group, the MHE model group 
      and the DA intervention model group had a significant increase in the relative 
      protein expression of TAAR1 (3.72 +/- 0.50/4.18 +/- 0.43 vs 0.96 +/- 0.40, both P < 
      0.05) and a significant reduction in the expression of EAAT2 (0.46 +/- 0.16/0.51 +/- 
      0.20 vs 0.92 +/- 0.11, P = 0.013 and 0.036). Compared with the model group treated 
      with empty vector, the MHE model group and the DA intervention model group had a 
      significant increase in the relative protein expression of EAAT2 after TAAR1 
      siRNA intervention (0.86+/-0.142 vs 0.56 +/- 0.060, P = 0.028; 0.99 +/- 0.056 vs 0.43 +/- 
      0.098, P = 0.0010) and a significant reduction in the extracellular Glu level in 
      the brain at 60-120 minutes after injection, while after TAAR1 plasmid 
      intervention, the MHE model group and the DA intervention model group had a 
      significant reduction in the relative protein expression of EAAT2 (0.20 +/- 0.040 
      vs 0.48 +/- 0.08, P = 0.006; 0.24 +/- 0.05 vs 0.54 +/- 0.07, P = 0.004) and a 
      significant increase in the extracellular Glu level in brain at 60-100 minutes 
      after injection. Conclusion: DA interacts with TAAR1 in brain tissue to induce 
      extracellular accumulation of Glu, thus leading to the disorder of the 
      TAAR1-EAAT2 signaling pathway in brain tissue and ultimately injuring the 
      cognitive function of MHE rats.
FAU - Wen, F F
AU  - Wen FF
AD  - Zhejiang Provincial Key Laboratory of Aging and Neurological Disease Research, 
      the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, 
      China.
FAU - Xu, Z
AU  - Xu Z
AD  - Neurosurgery Department, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Liu, L P
AU  - Liu LP
AD  - Surgery Laboratory, the First Affiliated Hospital of Wenzhou Medical University, 
      Wenzhou 325000, China.
FAU - Yang, J J
AU  - Yang JJ
AD  - Neurosurgery Department, the First Affiliated Hospital of Wenzhou Medical 
      University, Wenzhou 325000, China.
FAU - Ding, S D
AU  - Ding SD
AD  - Zhejiang Provincial Key Laboratory of Aging and Neurological Disease Research, 
      the First Affiliated Hospital of Wenzhou Medical University, Wenzhou 325000, 
      China.
LA  - chi
PT  - Journal Article
PL  - China
TA  - Zhonghua Gan Zang Bing Za Zhi
JT  - Zhonghua gan zang bing za zhi = Zhonghua ganzangbing zazhi = Chinese journal of 
      hepatology
JID - 9710009
RN  - 3KX376GY7L (Glutamic Acid)
RN  - VTD58H1Z2X (Dopamine)
SB  - IM
MH  - Animals
MH  - Astrocytes/metabolism
MH  - *Cognitive Dysfunction/pathology
MH  - Dopamine/*pharmacology
MH  - Glutamic Acid/drug effects/*metabolism
MH  - *Hepatic Encephalopathy/pathology
MH  - Neurons/*drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
OTO - NOTNLM
OT  - Dopamine
OT  - Glutamate
OT  - Hepatic encephalopathy
OT  - Rats
EDAT- 2018/05/29 06:00
MHDA- 2019/03/30 06:00
CRDT- 2018/05/28 06:00
PHST- 2018/05/28 06:00 [entrez]
PHST- 2018/05/29 06:00 [pubmed]
PHST- 2019/03/30 06:00 [medline]
AID - 10.3760/cma.j.issn.1007-3418.2018.01.011 [doi]
PST - ppublish
SO  - Zhonghua Gan Zang Bing Za Zhi. 2018 Jan 20;26(1):48-53. doi: 
      10.3760/cma.j.issn.1007-3418.2018.01.011.