Morphine Dependence is Attenuated by Treatment of 3,4,5-Trimethoxy Cinnamic Acid in Mice and Rats
- 주제(키워드) 3 , 4 , 5-Trimethoxy cinnamic acid (TMCA) , Morphine dependence , NMDA , Nucleus accumbens , FosB
- 주제(기타) Biochemistry & Molecular Biology; Neurosciences
- 설명문(일반) [Moon, Sohyeon; Kang, Seungmin; Sur, Bongjun; Oh, Seikwan] Ewha Womans Univ, Sch Med, Dept Mol Med, Seoul 07985, South Korea; [Shin, Heeyeon] St Louis Coll Pharm, St Louis, MO 63108 USA; [Yayeh, Taddesse] Bahir Dar Univ, Sch Anim & Vet Med, Dept Vet Med, POB 5501, Bahir Dar, Ethiopia
- 등재 SCIE, SCOPUS
- 발행기관 SPRINGER/PLENUM PUBLISHERS
- 발행년도 2019
- URI http://www.dcollection.net/handler/ewha/000000159818
- 본문언어 영어
- Published As http://dx.doi.org/10.1007/s11064-019-02720-9
- PubMed https://pubmed.ncbi.nlm.nih.gov/30632088
초록/요약
The effect of 3, 4, 5-trimethoxy cinnamic acid (TMCA) against morphine-induced dependence in mice and rats was investigated. Mice were pretreated with TMCA and then morphine was injected intraperitoneally; whereas rats were treated with TMCA (i.p.) and infused with morphine into the lateral ventricle of brain. Naloxone-induced morphine withdrawal syndrome and conditioned place preference test were performed. Moreover, western blotting and immunohistochemistry were used to measure protein expressions. Number of naloxone-precipitated jumps and conditioned place preference score in mice were attenuated by TMCA. Likewise, TMCA attenuated morphine dependent behavioral patterns such as diarrhea, grooming, penis licking, rearing, teeth chattering, and vocalization in rats. Moreover, the expression levels of pNR1and pERK in the frontal cortex of mice and cultured cortical neurons were diminished by TMCA. In the striatum, pERK expression was attenuated despite unaltered expression of pNR1 and NR1. Interestingly, morphine-induced elevations of FosB/FosB(+) cells were suppressed by TMCA (50, 100mg/kg) in the nucleus accumbens sub-shell region of mice. In conclusion, TMCA could be considered as potential therapeutic agent against morphine-induced dependence.
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