gabab受體在神經干細胞c17.2中的分子機制及功能研究

1、華中科技大學碩士學位論文GABAB受體在神經干細胞C17.2中的分子機制及功能研究姓名：金煒申請學位級別：碩士專業(yè)：生物化學與分子生物學指導教師：劉劍峰;殷慎敏2011-01-12華 中 科 技 大 學 碩 士 學 位 論 文 華 中 科 技 大 學 碩 士 學 位 論 文 Abstract Gamma-aminobutyric acid type B receptors (GABABR) are G-protein-couple

2、d receptors for the main inhibitory neurotransimitter in the brain.The metabotropic GABABR in GPCR family is very special, among G-protein coupled receptors,GABAB receptors are unique in that require GABAB1 and GABAB2 su

3、bunits assemble to form functional receptor and GABAB2 determine their subcellular localization. GABABR are implicated in a variety of physiological function,including neurological and psychiatric disorders and so on.We

4、found that receptor agonist baclofen inhibits neural stem cells c17.2 proliferation.Western blotting exhibit that GABAB receptor activation phoshorylate extracellular regulated protein kinases （ERK）,while lead to Src pho

5、sphorylation.These proteins phosphorylation will regulate a variety of physiological functions in neural stem cells,including inhibiting neual stem cells proliferation.In addition,we also noted that GABAB receptor activa

6、tion transactivate IGF receptors and protect neural stem cells from apoptosis. I also showed that CGP7930,a positive allosteric regulator specific for GABAB2,alone could lead to ERK1/2 phosphorylation.CGP54626, GABAB rec

7、eptor antagonist,could block effects of the agonist baclofen –induced Src/ERK1/2 / IGFR phosphorylation. AMPK inhibitor compound C can block agonist Metformin-induced cell inhibitory effect. GABAB receptor inhibitor CGP5

8、4626 could block the AMPK agonist Metformin-induced cell inhibitory effect. Taken together,GABABR regulate a series of signal pathway.This thesis is only a preliminary investigation for GABAB receptors of molecular mech