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Effect of dexmedetomidine on hippocampal neuron development and BDNF-TrkB signal expression in neonatal rats

Authors Lv J, Ou W, Zou XH, Yao Y, Wu JL

Received 18 August 2016

Accepted for publication 27 September 2016

Published 9 December 2016 Volume 2016:12 Pages 3153—3159

DOI https://doi.org/10.2147/NDT.S120078

Checked for plagiarism Yes

Review by Single-blind

Peer reviewers approved by Prof. Dr. Roumen Kirov

Peer reviewer comments 2

Editor who approved publication: Professor Wai Kwong Tang


Jie Lv, Wei Ou, Xiao-Hua Zou, Yin Yao, Jin-Li Wu

Department of Anesthesia, Guizhou Medical University Affiliated Hospital, Guiyang, People’s Republic of China

Abstract: The study aimed to explore the effect of dexmedetomidine (DEX) on hippocampal neuron development process and on molecular expression of brain-derived neurotrophic factor (BDNF)-tyrosine receptor kinase B (TrkB) signaling pathway in neonatal rats. The hippocampal neuron cells were isolated from newborn neonatal rats and cultured in vitro. One control group and three treated groups with 1, 10, and 100 µmol/L DEX were used for the study. Cell activity and apoptosis were detected by the MTT and terminal deoxynucleotidyl transferase-mediated biotinylated uridine triphosphate (UTP) nick end labeling assays. The synaptophysin (SYN) and postsynaptic density 95 (PSD95) were detected by quantitative polymerase chain reaction. There was no difference in the viability of neuron cells among the different dose groups of DEX and the control group during days 2-10 (P>0.05). Compared to the control group, there was no significant difference (P>0.05) in the expressions of SYN and PSD95 in the groups treated with 1 and 10 µmol/L DEX, whereas significant difference in the expression was observed in the group treated with 100 µmol/L DEX (P<0.01). Compared with the control group, the expression of BDNF was significantly upregulated (P<0.05) in the group treated with 100 µmol/L DEX. There were no significant differences in TrkB expression among the four groups. The expression of p-N-methyl-D-aspartate receptor increased with an increase in the concentration of DEX; however, only the high dose revealed a significant upregulation compared with the control group. The neuroprotective effect of DEX may be achieved by upregulating the expression of BDNF and phosphorylation level of N-methyl-D-aspartate receptor.

Keywords: dexmedetomidine, hippocampal neuron, development, BDNF-TrkB

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