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1. Selective alpha 1- and alpha 2-adrenoreceptor agonist on galanin expression in cultured dorsal root ganglion neurons | |||
LIU Zhen,LI Zhenzhong | |||
Basic Medicine 27 December 2012 | |||
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Abstract:In this paper, the effects of selective alpha 1- or alpha 2-adrenoreceptor agonist on galanin (Gal) expression in dorsal root ganglion (DRG) neurons were investigated. Alpha-adrenoreceptors are expressed in sympathetic neurons. Interestingly, functional alpha-adrenoreceptors are also expressed in DRG primary sensory neurons and regulate neurogenic inflammation and nociceptive responses. Gal is involved in inflammation and nociception. Whether selective alpha 1- or alpha 2-adrenoreceptor agonist affects Gal expression in DRG neurons is still unclear. In the present study, primary cultured DRG neurons were used to determine effects of alpha 1-adrenoreceptor agonist phenylephedrine (10-5 mol/L) or alpha 2-adrenoreceptor agonist clonidine (10-5 mol/L) on Gal and its mRNA expression. The results showed that alpha 1-adrenoreceptor agonist phenylephedrine promoted Gal mRNA and Gal peptide expression after 4 days incubation. Alpha 2-adrenoreceptor agonist clonidine did not have significant effect on Gal and its mRNA expression. These results imply that activation of alpha 1-adrenoreceptor, but not alpha 2-adrenoreceptor, was involved in Gal expression. These effects may be relevant to noradrenergic pain modulation. | |||
TO cite this article:LIU Zhen,LI Zhenzhong. Selective alpha 1- and alpha 2-adrenoreceptor agonist on galanin expression in cultured dorsal root ganglion neurons[OL].[27 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4509467 |
2. Exposure of selective beta 1- and beta 2-adrenoreceptor agonist or antagonist on galanin expression in sympathetic neurons in vitro | |||
LIU Zhen,LI Zhenzhong | |||
Basic Medicine 27 December 2012 | |||
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Abstract:In this paper, the possible regulation of selective beta 1- and beta 2-adrenoreceptor agonists or antagonists on galanin (Gal) expression in organotypically cultured superior cervical ganglion (SCG) neurons was evaluated. Gal, a 29-amino-acid neuropeptide in most species (30-amino-acid in human), is expressed in SCG neurons and plays a trophic role in the adult animal and acts as an inhibitory modulator of cholinergic and noradrenergic neurotransmission. Whether beta-adrenoreceptors are involved in modulation on Gal expression in SCG neurons remains unknown. In the present study, after acute (4 hours) or chronic (4 days) incubation with these agonists or antagonists, the expression of Gal and its mRNA were estimated by double fluorescent labeling and real time-PCR, respectively. The results showed that the amount of Gal and Gal mRNA expression in organotypically cultured SCG neurons decreased significantly after chronic stimulation with beta 2-adrenoreceptor agonist salbutamol as compared with that in control group. Beta 1-adrenoreceptor agonist denopamine, antagonist metoprolol, and beta 2-adrenoreceptor antagonist ICI118551 chronic stimulation did not have effects on Gal and Gal mRNA expression. The expression of Gal and its mRNA did not significantly change after acute exposure of these agents. These data implicated that Gal may be regulated by chronic activation beta 2-adrenoreceptors, but not beta 1-adrenoreceptors in sympathetic neurons. | |||
TO cite this article:LIU Zhen,LI Zhenzhong. Exposure of selective beta 1- and beta 2-adrenoreceptor agonist or antagonist on galanin expression in sympathetic neurons in vitro[OL].[27 December 2012] http://en.paper.edu.cn/en_releasepaper/content/4509464 |
3. Valproate induces upregulation of Wnt/β-catenin pathway through DNA demethylation in primary cultured neurons | |||
Wang Zhongping,Chen Mingjun,Xu Li,Li Ruixi | |||
Basic Medicine 20 January 2011 | |||
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Abstract:Valproate (valproic acid, VPA) has been well used in treatment of the epilepsy. However, maternal administration of VPA early in pregnancy will remarkably increase susceptibility in the offspring to autism spectrum disorders (ASDs). It is proposed that dysregulation of Wnt/β-catenin pathway is an underlying mechanism. In the present study we observed that VPA treatment in primary cultured neurons significantly induced demethylation in the promoter region of the gene of wnt1 but not Wnt inhibitory factor -1 (WIF-1). Wnt1 mRNA expression was concomitantly increased, displaying correlation with the promoter region demethylation level. Furthermore, western blot showed significant overexpression of Wnt1 and β-catenin in the VPA treated neurons compared with control. We also observed that VPA treatment promoted neuronal growth, manifesting as significant increment of number of neurite branches and total neurite length in comparison with control neurons. We concluded that VPA induced upregulation of Wnt/β-catenin pathway through DNA demethylation in primary cultured neurons and further promotes neuronal neurite complexity. | |||
TO cite this article:Wang Zhongping,Chen Mingjun,Xu Li, et al. Valproate induces upregulation of Wnt/β-catenin pathway through DNA demethylation in primary cultured neurons[OL].[20 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4407902 |
4. Changes of the expression of β-catenin and GSK-3β in the brain in an autism model of rat | |||
Chen Mingjun,Wang Zhongping,Li Ruixi,Xu Li | |||
Basic Medicine 18 January 2011 | |||
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Abstract:In order to understand the role of the Wnt signal pathway in the etiology of the autism, the present study examined the expression of two signaling proteins, β-catenin and GSK-3β which take the key position in Wnt pathway, in the prefrontal cortex, hippocampus and cerebellum of an autism model of rat with different ages by means of the western blot technique. The results showed that the expression of the β-catenin was up-regulated, while the expression of the GSK-3β was decreased severely in the brain regions mentioned above in autism animal model. These results indicated that the Wnt signal pathway is over activated in the autism models, and this activation might be the one of the causes of abnormal development of neurons in the brain of autism. Therefore, the present results suggested that Wnt signal pathway plays an important role in the etiology of the autism. | |||
TO cite this article:Chen Mingjun,Wang Zhongping,Li Ruixi, et al. Changes of the expression of β-catenin and GSK-3β in the brain in an autism model of rat[OL].[18 January 2011] http://en.paper.edu.cn/en_releasepaper/content/4405800 |
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