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中国应用生理学杂志 ›› 2016, Vol. 32 ›› Issue (6): 487-493.doi: 10.13459/j.cnki.cjap.2016.06.002

• 研究论文 • 上一篇    下一篇

Modulation by desensitized nicotinic receptors on metabolism of DA in striatum derived from the hemiparkinsonian model

Fu-rong HAN1,2, Hai WANG2,3   

  1. 1. Department of Pharmacy, Beijing Tongren Hospital, Capital Medicine University, Beijing 100730, China;
    2. Cardiovascular Drug Research Center, Academy of Military Medical Sciences, Beijing 100850, China;
    3. Cardiovascular Drug Research Center, Thadweik Academy of Medicine, Beijing 100039, China
  • 收稿日期:2016-10-13 修回日期:2016-11-11 出版日期:2016-11-28 发布日期:2018-06-19
  • 通讯作者: Hai WANG,MD,Professor,Cardiovascular Drug Research Center,Academy of Military Medical Sciences,Thadweik Academy of Medicine,Beijing 100850,China,Tel:86-10-932651;E-mail:wh9588@sina.com E-mail:wh9588@sina.com

Modulation by desensitized nicotinic receptors on metabolism of DA in striatum derived from the hemiparkinsonian model

Fu-rong HAN1,2, Hai WANG2,3   

  1. 1. Department of Pharmacy, Beijing Tongren Hospital, Capital Medicine University, Beijing 100730, China;
    2. Cardiovascular Drug Research Center, Academy of Military Medical Sciences, Beijing 100850, China;
    3. Cardiovascular Drug Research Center, Thadweik Academy of Medicine, Beijing 100039, China
  • Received:2016-10-13 Revised:2016-11-11 Online:2016-11-28 Published:2018-06-19

摘要: Objective: The purpose of this study was to investigate the effects of desensitized nicotinic receptors (nAChRs) on striatal dopaminergic system in the hemiparkinsonian rats treated with 6-hydroxydopamine (6-OHDA). Methods: We examined the effects of desensitized nAChRs on the levels of dopamine (DA) and its metabolites, mRNA expression of dopamine receptor D1,D2 and monoamine oxidase B (MAO-B) in the striatum of 6-OHDA-lesioned rats using high-performance liquid chromatography and reverse transcription-polymerase chain reaction. Results: The results showed that nAChRs desensitization following repeated nicotine stimulation could reverse significantly the decrease of striatal DA and its metabolites levels and the increase in DA turnover in lesioned side striatum of hemiparkinsonian rats. Dopamine D1 receptor mRNA expression increased significantly, whereas dopamine D2 receptor mRNA expression remained unchanged in lesioned side striatum of nicotine-treated rats compared to 6-OHDA-lesioned rats when nAChRs were desensitized. Meanwhile, nicotine-treated rats displayed a significant decrease in MAO-B mRNA expression in lesioned side striatum compared to 6-OHDA-lesioned rats after nAChRs desensitization. Conclusion: These results suggest that nAChRs desensitization could promote DA level, upregulate dopamine D1 receptor expression and downregulate MAO-B expression in striatum of hemiparkinsonian rats.

关键词: Parkinson's disease, nicotine, nicotine acetylcholine receptor, desensitization

Abstract: Objective: The purpose of this study was to investigate the effects of desensitized nicotinic receptors (nAChRs) on striatal dopaminergic system in the hemiparkinsonian rats treated with 6-hydroxydopamine (6-OHDA). Methods: We examined the effects of desensitized nAChRs on the levels of dopamine (DA) and its metabolites, mRNA expression of dopamine receptor D1,D2 and monoamine oxidase B (MAO-B) in the striatum of 6-OHDA-lesioned rats using high-performance liquid chromatography and reverse transcription-polymerase chain reaction. Results: The results showed that nAChRs desensitization following repeated nicotine stimulation could reverse significantly the decrease of striatal DA and its metabolites levels and the increase in DA turnover in lesioned side striatum of hemiparkinsonian rats. Dopamine D1 receptor mRNA expression increased significantly, whereas dopamine D2 receptor mRNA expression remained unchanged in lesioned side striatum of nicotine-treated rats compared to 6-OHDA-lesioned rats when nAChRs were desensitized. Meanwhile, nicotine-treated rats displayed a significant decrease in MAO-B mRNA expression in lesioned side striatum compared to 6-OHDA-lesioned rats after nAChRs desensitization. Conclusion: These results suggest that nAChRs desensitization could promote DA level, upregulate dopamine D1 receptor expression and downregulate MAO-B expression in striatum of hemiparkinsonian rats.

Key words: Parkinson's disease, nicotine, nicotine acetylcholine receptor, desensitization

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