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Effects of sodium butyrate in animal models of mania and depression
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What this work says
Outgoing claims: the papers this work cites, builds on, or argues with.
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The Na,K-ATPase hypothesis for manic-depression. I. General considerations
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Behavioral and neurochemical effects of sodium butyrate in an animal model of mania
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Three times more days depressed than manic or hypomanic in both bipolar I and bipolar II disorder 1
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Folic acid administration prevents ouabain‐induced hyperlocomotion and alterations in oxidative stress markers in the rat brain
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The HDAC inhibitor, sodium butyrate, stimulates neurogenesis in the ischemic brain
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Dopamine dysregulation syndrome: implications for a dopamine hypothesis of bipolar disorder
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Functions of Site-Specific Histone Acetylation and Deacetylation
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Chronic Mild Stress (CMS) Revisited: Consistency and Behavioural-Neurobiological Concordance in the Effects of CMS
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Linking Molecules to Mood: New Insight Into the Biology of Depression
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HDAC6 Regulates Mitochondrial Transport in Hippocampal Neurons
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Regulation of Neurogenesis and Gliogenesis by Stress and Antidepressant Treatment
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Antidepressant-like effect of sodium butyrate (HDAC inhibitor) and its molecular mechanism of action in the rat hippocampus
What points at this work
Incoming claims: where this work appears in other papers’ reference lists and arguments.
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