Valproic acid induces up- or down-regulation of gene expression responsible for the neuronal excitation and inhibition in rat cortical neurons through its epigenetic actions

@article{Fukuchi2009ValproicAI,
  title={Valproic acid induces up- or down-regulation of gene expression responsible for the neuronal excitation and inhibition in rat cortical neurons through its epigenetic actions},
  author={Mamoru Fukuchi and Takuya Nii and Naoki Ishimaru and Aya Minamino and Daichi Hara and Ichiro Takasaki and Akiko Tabuchi and Masaaki Tsuda},
  journal={Neuroscience Research},
  year={2009},
  volume={65},
  pages={35-43}
}
Transcriptional analysis of sodium valproate in a serotonergic cell line reveals gene regulation through both HDAC inhibition-dependent and independent mechanisms
TLDR
Results suggest VPA may regulate genes through both HDAC-dependent and independent mechanisms, as well as highlighting molecular processes that may underlie regulation of mood.
Transcriptional analysis of sodium valproate in a serotonergic cell line reveals gene regulation through both HDAC inhibition-dependent and independent mechanisms.
TLDR
Results suggest VPA may regulate genes through both HDAC-dependent and independent mechanisms, as well as highlighting molecular processes that may underlie regulation of mood.
Epigenetic Downregulation of Scn3a Expression by Valproate: a Possible Role in Its Anticonvulsant Activity
TLDR
An epigenetic pathway for the VPA-induced downregulation of Scn3a expression is suggested, which provides a possible role of this pathway in the anticonvulsant action of VPA.
Downregulation of TrkB Expression and Signaling by Valproic Acid and Other Histone Deacetylase Inhibitors
TLDR
Exposure to valproic acid is shown to downregulate TrkB expression and functional activity in retinoic acid-differentiated human neuroblastoma cell lines and primary mouse cortical neurons, providing evidence that this effect implicates relevant consequences with regard to BDNF efficacy in stimulating intracellular signaling and functional responses.
Valproate-Induced Epigenetic Upregulation of Hypothalamic Fto Expression Potentially Linked with Weight Gain
TLDR
It is shown that VPA increases the Fto mRNA and protein expression in mouse hypothalamic GT1-7 cells, suggesting an involvement of VPA in the epigenetic upregulation of hypothalamic FTO expression that is potentially associated with the VPA-induced weight gain.
Valproic acid mediates the synaptic excitatory/inhibitory balance through astrocytes — A preliminary study
Valproic acid mediates miR-124 to down-regulate a novel protein target, GNAI1
Valproic Acid Induces Telomerase Reverse Transcriptase Expression during Cortical Development
TLDR
Experimental evidence is provided that telomerase reverse transcriptase (TERT), a protein component of ribonucleoproteins complex of telomersase, is involved in the abnormal components caused by VPA in addition to Pax6 and its downstream signals and has important implications for the role of TERT as a modulator of balanced neuronal development and transmission in the brain.
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TLDR
It is proposed that inhibition of histone deacetylase provides a mechanism for valproic acid-induced birth defects and could also explain the efficacy of valproIC acid in the treatment of bipolar disorder.
The mood stabilizer valproic acid stimulates GABA neurogenesis from rat forebrain stem cells
TLDR
The enhancement of GABAergic neuron numbers, neurite outgrowth, and phenotypic expression via increases in the neuronal differentiation of neural stem cell may contribute to the therapeutic effects of valproate in the treatment of bipolar disorder.
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TLDR
It is found that chronic treatment of rats with valproate increased levels of activated phospho-ERK44/42 in neurons of the anterior cingulate, a region in whichValproate-induced increases in expression of an ERK pathway-regulated gene, bcl-2, demonstrate that valproates activates the ERK route and induces ERK pathways-mediated neurotrophic actions.
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Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease
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TLDR
Preclinical trials with suberoylanilide hydroxamic acid (SAHA), a potent HDAC inhibitor, show that SAHA crosses the blood–brain barrier and increases histone acetylation in the brain, clearly validating the pursuit of this class of compounds as HD therapeutics.
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