Search

Your search keyword '"Ma, Ze-Gang"' showing total 26 results
Start Over Author "Ma, Ze-Gang"
26 results on '"Ma, Ze-Gang"'

13. Cocaine potently blocks neuronal α3β4nicotinic acetylcholine receptors in SH-SY5Y cells

Author

Ma, Ze-gang, Jiang, Nan, Huang, Yuan-bing, Ma, Xiao-kuang, Brek Eaton, Jason, Gao, Ming, Chang, Yong-chang, Lukas, Ronald J, Whiteaker, Paul, Neisewander, Janet, and Wu, Jie

Abstract

Cocaine is one of the most abused illicit drugs worldwide. It is well known that the dopamine (DA) transporter is its major target; but cocaine also acts on other targets including nicotinic acetylcholine receptors (nAChRs). In this study, we investigated the effects of cocaine on a special subtype of neuronal nAChR, α3β4-nAChR expressed in native SH-SY5Y cells. α3β4-nAChR-mediated currents were recorded using whole-cell recordings. Drugs were applied using a computer-controlled U-tube drug perfusion system. We showed that bath application of nicotine induced inward currents in a concentration-dependent manner with an EC50value of 20 µM. Pre-treatment with cocaine concentration-dependently inhibited nicotine-induced current with an IC50of 1.5 μM. Kinetic analysis showed that cocaine accelerated α3β4-nAChR desensitization, which caused a reduction of the amplitude of nicotine-induced currents. Co-application of nicotine and cocaine (1.5 μM) depressed the maximum response on the nicotine concentration-response curve without changing the EC50value, suggesting a non-competitive mechanism. The cocaine-induced inhibition of nicotine response exhibited both voltage- and use-dependence, suggesting an open-channel blocking mechanism. Furthermore, intracellular application of GDP-βS (via recording electrode) did not affect cocaine-induced inhibition, suggesting that cocaine did not alter receptor internalization. Moreover, intracellular application of cocaine (30 µM) failed to alter the nicotine response. Finally, cocaine (1.5 μM) was unable to inhibit the nicotine-induced inward current in heterologous expressed α6/α3β2β3-nAChRs and α4β2-nAChRs expressed in human SH-EP1 cells. Collectively, our results suggest that cocaine is a potent blocker for native α3β4-nAChRs expressed in SH-SY5Y cells.

Published
2020
Full Text
View/download PDF

15. Flavonoid Myricetin Modulates G A B A A Receptor Activity through Activation of Ca 2+ Channels and CaMK-II Pathway

Author

Zhang, Xiao Hu, Ma, Ze Gang, Rowlands, Dewi Kenneth, Gou, Yu Lin, Fok, Kin Lam, Wong, Hau Yan, Yu, Mei Kuen, Tsang, Lai Ling, Mu, Li, Chen, Lei, Yung, Wing Ho, Chung, Yiu Wa, Zhang, Bei Lin, Zhao, Hua, and Chan, Hsiao Chang

Subjects
endocrine system, nervous system, Research Article
Abstract

The flavonoid myricetin is found in several sedative herbs, for example, the St. John's Wort, but its influence on sedation and its possible mechanism of action are unknown. Using patch-clamp technique on a brain slice preparation, the present study found that myricetin promoted GABAergic activity in the neurons of hypothalamic paraventricular nucleus (PVN) by increasing the decay time and frequency of the inhibitory currents mediated by GABA(A) receptor. This effect of myricetin was not blocked by the GABA(A) receptor benzodiazepine- (BZ-) binding site antagonist flumazenil, but by KN-62, a specific inhibitor of the Ca(2+)/calmodulin-stimulated protein kinase II (CaMK-II). Patch clamp and live Ca(2+) imaging studies found that myricetin could increase Ca(2+) current and intracellular Ca(2+) concentration, respectively, via T- and L-type Ca(2+) channels in rat PVN neurons and hypothalamic primary culture neurons. Immunofluorescence staining showed increased phosphorylation of CaMK-II after myricetin incubation in primary culture of rat hypothalamic neurons, and the myricetin-induced CaMK-II phosphorylation was further confirmed by Western blotting in PC-12 cells. The present results suggest that myricetin enhances GABA(A) receptor activity via calcium channel/CaMK-II dependent mechanism, which is distinctively different from that of most existing BZ-binding site agonists of GABA(A) receptor.

Published
2012

16. Flavonoid Myricetin Modulates GABAA Receptor Activity through Activation of Ca2+ Channels and CaMK-II Pathway

Author

Zhang, Xiao Hu, Ma, Ze Gang, Rowlands, Dewi Kenneth, Gou, Yu Lin, Fok, Kin Lam, Wong, Hau Yan, Yu, Mei Kuen, Tsang, Lai Ling, Mu, Li, Chen, Lei, Yung, Wing Ho, Chung, Yiu Wa, Zhang, Bei Lin, Zhao, Hua, and Chan, Hsiao Chang

Subjects
endocrine system, Article Subject, nervous system, lcsh:Other systems of medicine, lcsh:RZ201-999
Abstract

The flavonoid myricetin is found in several sedative herbs, for example, the St. John's Wort, but its influence on sedation and its possible mechanism of action are unknown. Using patch-clamp technique on a brain slice preparation, the present study found that myricetin promoted GABAergic activity in the neurons of hypothalamic paraventricular nucleus (PVN) by increasing the decay time and frequency of the inhibitory currents mediated by GABAA receptor. This effect of myricetin was not blocked by the GABAA receptor benzodiazepine- (BZ-) binding site antagonist flumazenil, but by KN-62, a specific inhibitor of the Ca2+/calmodulin-stimulated protein kinase II (CaMK-II). Patch clamp and live Ca2+ imaging studies found that myricetin could increase Ca2+ current and intracellular Ca2+ concentration, respectively, via T- and L-type Ca2+ channels in rat PVN neurons and hypothalamic primary culture neurons. Immunofluorescence staining showed increased phosphorylation of CaMK-II after myricetin incubation in primary culture of rat hypothalamic neurons, and the myricetin-induced CaMK-II phosphorylation was further confirmed by Western blotting in PC-12 cells. The present results suggest that myricetin enhances GABAA receptor activity via calcium channel/CaMK-II dependent mechanism, which is distinctively different from that of most existing BZ-binding site agonists of GABAA receptor.

Published
2012

20. Flavonoid Myricetin ModulatesGABAAReceptor Activity through Activation ofCa2+Channels and CaMK-II Pathway

Author

Zhang, Xiao Hu, primary, Ma, Ze Gang, additional, Rowlands, Dewi Kenneth, additional, Gou, Yu Lin, additional, Fok, Kin Lam, additional, Wong, Hau Yan, additional, Yu, Mei Kuen, additional, Tsang, Lai Ling, additional, Mu, Li, additional, Chen, Lei, additional, Yung, Wing Ho, additional, Chung, Yiu Wa, additional, Zhang, Bei Lin, additional, Zhao, Hua, additional, and Chan, Hsiao Chang, additional

Published
2012
Full Text
View/download PDF

24. HLA-DRA rs3129882 A/G polymorphism was not a risk factor for Parkinson's disease in Chinese-based populations: a meta-analysis.

Author

Ma, Ze-Gang, Liu, Tian-Wei, and Bo, Yong-Li

Subjects
*DISEASE risk factors, *PARKINSON'S disease, *HLA histocompatibility antigens, *SINGLE nucleotide polymorphisms, *MESSENGER RNA, *GENOTYPES, *RNA splicing, *META-analysis, HEALTH of Chinese people
Abstract

Purpose: Many studies have evaluated the association between the HLA-DRA rs3129882 A/G polymorphism and risk for Parkinson's disease (PD) in Chinese-based populations, however, published data remain inconclusive. Therefore, we performed a meta-analysis from all relevant studies to evaluate an association of HLA-DRA rs3129882 A/G polymorphism with susceptibility to PD. Methods: The summary odds ratio (OR) with its 95% confidence interval (CI) was calculated to evaluate the association. The Q statistic was used to evaluate homogeneity and funnel plots were used to assess publication bias. The minor A allele frequencies, additive, dominant as well as recessive genetic models were examined in the analyses. Results: Five case-control studies with a total of 2230 PD cases and 2262 controls from Mainland China, Taiwan, Singapore, and Malaysia were included in the final meta-analysis. Neither the minor A allele frequencies nor the genotypic distributions were significantly different between PD cases and controls when all studies were pooled into this meta-analysis. Conclusion: The results of this meta-analysis suggest that HLA-DRA rs3129882 A/G polymorphism was not responsible for PD in Chinese-based populations. [ABSTRACT FROM AUTHOR]

Published
2015
Full Text
View/download PDF

Catalog

Books, media, physical & digital resources
See catalog results