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학술저널
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Xing, Yi (Department of Neurosurgery, Shandong University Affi liated Shandong Provincial Hospital) Chen, Xiuying (Department of Electroencephalography, Shandong University Affi liated Shandong Provincial Hospital) Liu, Zhen (Department of Anatomy, Shandong University School of Medicine) Li, Hao (Department of Anatomy, Shandong University School of Medicine) Liu, Huaxiang (Department of Rheumatology, Shandong University Qilu Hospital) Li, Zhenzhong (Department of Anatomy, Shandong University School of Medicine)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제19권 제3호
발행연도
2011.1
수록면
315 - 319 (5page)

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Galanin (Gal) is a 29-amino-acid neuropeptide which is expressed in superior cervical ganglion (SCG) neurons and plays a trophic role in the adult animal and acts as an inhibitory modulator of cholinergic and noradrenergic neurotransmission. Whether activation or inhibition of alpha-adrenoreceptors infl uences Gal mRNA expression in SCG neurons remains unknown. Here, we have evaluated the possible regulation of Gal mRNA expression with acute (4 h) and chronic (4 days) stimulation of alpha 1- and alpha 2-adrenoreceptor agonists or antagonists in primary cultured SCG neurons. The results showed that the amount of Gal mRNA expression in cultured SCG neurons increased signifi cantly after chronic stimulation with alpha 2-adrenoreceptor antagonist yohimbine compared with control SCG neurons at the same time point, whereas the amount of Gal mRNA expression decreased signifi cantly after chronic stimulation with alpha 2-adrenoreceptor agonist clonidine as compared with that in control group. All these effects were not dose-dependent on the administration of alpha 2-adrenoreceptor agonist clonidine or alpha 2-adrenoreceptor antagonist yohimbine. Alpha 1-adrenoreceptor agonist phenylephrine or antagonist prazosin chronic stimulation did not have effects on Gal mRNA expression. Acute exposure of these agents did not have effects on Gal mRNA expression. The present study showed that Gal may be regulated by activation or inhibition of alpha 2-adrenoreceptors, but not alpha 1-adrenoreceptors in sympathetic neurons.

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