short-term striatal gene expression responses to brain-derived neurotrophic factor are dependent on mek and erk activation短期内纹状体脑源性神经营养因子基因表达反应依赖于mek和erk激活.pdfVIP

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short-term striatal gene expression responses to brain-derived neurotrophic factor are dependent on mek and erk activation短期内纹状体脑源性神经营养因子基因表达反应依赖于mek和erk激活.pdf

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short-term striatal gene expression responses to brain-derived neurotrophic factor are dependent on mek and erk activation短期内纹状体脑源性神经营养因子基因表达反应依赖于mek和erk激活

Short-Term Striatal Gene Expression Responses to Brain- Derived Neurotrophic Factor Are Dependent on MEK and ERK Activation Ozgun Gokce, Heike Runne, Alexandre Kuhn, Ruth Luthi-Carter* ´ ´ ´ Laboratory of Functional Neurogenomics, Brain Mind Institute, Ecole Polytechnique Federale de Lausanne (EPFL), Lausanne, Switzerland Abstract Background: Brain-derived neurotrophic factor (BDNF) is believed to be an important regulator of striatal neuron survival, differentiation, and plasticity. Moreover, reduction of BDNF delivery to the striatum has been implicated in the pathophysiology of Huntington’s disease. Nevertheless, many essential aspects of BDNF responses in striatal neurons remain to be elucidated. Methodology/Principal Findings: In this study, we assessed the relative contributions of multipartite intracellular signaling pathways to the short-term induction of striatal gene expression by BDNF. To identify genes regulated by BDNF in these GABAergic cells, we first used DNA microarrays to quantify their transcriptomic responses following 3 h of BDNF exposure. The signal transduction pathways underlying gene induction were subsequently dissected using pharmacological agents and quantitative real-time PCR. Gene expression responses to BDNF were abolished by inhibitors of TrkB (K252a) and calcium (chelator BAPTA-AM and transient receptor potential cation channel [TRPC] antagonist SKF-96365). Interestingly, inhibitors of mitogen-activated protein kinase kinases 1 and 2 (MEK1/2) and extracellular signal-regulated kinase ERK also blocked the BDNF-mediated induction of all tested BDNF-responsive genes. In contrast, inhibitors of nitric oxide synthase (NOS), phosphotidylinositol-3-kinase (PI3K), and CAMK exhibited