ArticlePloS one2009
Short-term striatal gene expression responses to brain-derived neurotrophic factor are dependent on MEK and ERK activation.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 54 citations in OpenAlex.
- Article
- Anaesthetic-dependent changes in gene expression following acute and chronic exposure in the rodent brain.Scientific reports · 2020Article
- Dopamine D1 and Glutamate Receptors Co-operate With Brain-Derived Neurotrophic Factor (BDNF) and TrkB to Modulate ERK Signaling in Adult Striatal Slices.Frontiers in cellular neuroscience · 2020Article
- NT-4/5 antagonizes the BDNF modulation of corticostriatal transmission: Role of the TrkB.T1 receptor.CNS neuroscience & therapeutics · 2019Article
- The Bu Shen Yi Sui Formula Promotes Axonal RegenerationFrontiers in pharmacology · 2019Article
- Fully human agonist antibodies to TrkB using autocrine cell-based selection from a combinatorial antibody library.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Large-scale transcriptomic analysis reveals that pridopidine reverses aberrant gene expression and activates neuroprotective pathways in the YAC128 HD mouse.Molecular neurodegeneration · 2018Article
- ESC-Derived BDNF-Overexpressing Neural Progenitors Differentially Promote Recovery in Huntington's Disease Models by Enhanced Striatal Differentiation.Stem cell reports · 2016Article
- Pridopidine activates neuroprotective pathways impaired in Huntington Disease.Human molecular genetics · 2016Article
- Trk inhibition reduces cell proliferation and potentiates the effects of chemotherapeutic agents in Ewing sarcoma.Oncotarget · 2016Article
- Impaired TrkB Signaling Underlies Reduced BDNF-Mediated Trophic Support of Striatal Neurons in the R6/2 Mouse Model of Huntington's Disease.Frontiers in cellular neuroscience · 2016Article
- An evaluation of the effects of acute and chronic L-tyrosine administration on BDNF levels and BDNF mRNA expression in the rat brain.Molecular neurobiology · 2014Article
- MAP kinase phosphatase 1 (MKP-1/DUSP1) is neuroprotective in Huntington's disease via additive effects of JNK and p38 inhibition.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Egr-1 induces DARPP-32 expression in striatal medium spiny neurons via a conserved intragenic element.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- A novel target for Huntington's disease: ERK at the crossroads of signaling. The ERK signaling pathway is implicated in Huntington's disease and its upregulation ameliorates pathology.BioEssays : news and reviews in molecular, cellular and developmental biology · 2012Article
- Nanoparticle-mediated signaling endosome localization regulates growth cone motility and neurite growth.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Necrostatin-1 ameliorates symptoms in R6/2 transgenic mouse model of Huntington's disease.Cell death & disease · 2011Article
- A point mutation in the dynein heavy chain gene leads to striatal atrophy and compromises neurite outgrowth of striatal neurons.Human molecular genetics · 2010Article
- The role of transient receptor potential cation channels in Ca2+ signaling.Cold Spring Harbor perspectives in biology · 2010Article
- TRPC channels and their implication in neurological diseases.CNS & neurological disorders drug targets · 2010Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBrain-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
findingsIn 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 less prevalent, gene-specific effects on BDNF-induced RNA expression. At the nuclear level, the activation of both Elk-1 and CREB showed MEK dependence. Importantly, MEK-dependent activation of transcription was shown to be required for BDNF-induced striatal neurite outgrowth, providing evidence for its contribution to striatal neuron plasticity.
conclusionsThese results show that the MEK/ERK pathway is a major mediator of neuronal plasticity and other important BDNF-dependent striatal functions that are fulfilled through the positive regulation of gene expression.
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