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

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.

Update on the Mechanism and Treatment of Sevoflurane-Induced Postoperative Cognitive Dysfunction

“…In addition, Dex enhances the cholinergic anti-inflammatory pathway via α7nAChR ( Carr et al, 2018 ). The neuroprotective effect of Dex may be achieved by upregulating BDNF expression ( Lv et al, 2016 ).…”

Dexmedetomidine prevents desflurane‐induced motor neuron death through NF‐KappaB pathway

“…Dexmedetomidine is widely used as an auxiliary drug in clinical anaesthesia. Previous study indicated that Dexmedetomidine could increase the BDNF expression in hippocampal neurons, implying that Dexmedetomidine may have a protective role in neurons. This was also confirmed by the finding that Dexmedetomidine increased acetylation level of histone in dopamine neurons, which was a molecular mechanism underlying the neuroprotective role of Dexmedetomidine .…”

Dexmedetomidine inhibits the PSD95‑NMDA receptor interaction to promote functional recovery following traumatic brain injury

“…Dexmedetomidine (Dex), which is an alpha-2 adrenergic receptor agonist drug, has been approved by the Food and Drug Administration (FDA) and is known for its anaesthetic, analgesic and neuroprotective effects ( 15 ). Dex also exerts a positive impact on neuronal development by regulating PSD95expression ( 16 ); however, the role of Dex in post-TBI neuroprotection remains unknown. The present study investigated the effect of Dex on the PSD95-NMDA interaction and subsequent functional recovery post-TBI.…”