Effect of Sinomenine on the Morphine-Dependence and Related Neural Mechanisms in Mice

Miao Fang, Junkui Li, Daoqi Zhu, Chaohua Luo, Chan Li, Chen Zhu, Menglin Fan, Kin Lam YUNG, Zhixian Mo*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

16 Citations (Scopus)


Evidence suggests that the dopamine receptor rate-limiting enzyme, tyrosine hydroxylase (TH), and the glutamate receptor, N-methyl-d-aspartate receptor 2B (NR2B), contribute to morphine dependence. Previous studies show that chronic exposure to morphine changes the expression of opioid receptors. In this study, we focus on the effects of sinomenine on morphine-dependent mice and its related neural mechanisms. Conditioned place preference (CPP) mouse model was established using morphine (9 mg/kg, s.c.), and their expression levels of TH and NR2B were observed by immunohistochemistry. Moreover, their mu opioid receptor (MOR) and delta opioid receptor (DOR) contents were assessed using quantitative reverse transcription polymerase chain reaction. Results showed that high sinomenine dose (80 mg/kg) effectively attenuated the behavior of CPP mice and reversed increased expression levels of TH and NR2B induced by morphine. Moreover, compared with the morphine group, sinomenine up-regulated the content of MOR to a normal level but did not significantly affect the DOR expression. In summary, these data indicate that sinomenine can inhibit morphine dependence by increasing the expression levels of TH, NR2B, and MOR in the mouse brain; however, DOR may not contribute to this effect.

Original languageEnglish
Pages (from-to)3587-3596
Number of pages10
JournalNeurochemical Research
Issue number12
Publication statusPublished - 1 Dec 2017

Scopus Subject Areas

  • Biochemistry
  • Cellular and Molecular Neuroscience

User-Defined Keywords

  • Morphine dependence
  • N-Methyl-d-aspartate receptor 2B
  • Opioid receptor
  • Sinomenine
  • Tyrosine hydroxylase


Dive into the research topics of 'Effect of Sinomenine on the Morphine-Dependence and Related Neural Mechanisms in Mice'. Together they form a unique fingerprint.

Cite this