The HDAC inhibitor, sodium butyrate, stimulates neurogenesis in the ischemic brain
Open accessAbstract
In the healthy adult brain, neurogenesis normally occurs in the subventricular zone (SVZ) and hippocampal dentate gyrus (DG). Cerebral ischemia enhances neurogenesis in neurogenic and non‐neurogenic regions of the ischemic brain of adult rodents. This study demonstrated that post‐insult treatment with a histone deacetylase inhibitor, sodium butyrate (SB), stimulated the incorporation of bromo‐2′‐deoxyuridine (BrdU) in the SVZ, DG, striatum, and frontal cortex in the ischemic brain of rats subjected to permanent cerebral ischemia. SB treatment also increased the number of cells expressing polysialic acid–neural cell adhesion molecule, nestin, glial fibrillary acidic protein, phospho‐cAMP response element‐binding protein (CREB), and brain‐derived neurotrophic factor (BDNF) in various brain regions after cerebral ischemia. Furthermore, extensive co‐localization of BrdU and polysialic acid–neural cell adhesion molecule was observed in multiple regions after ischemia, and SB treatment up‐regulated protein levels of BDNF, phospho‐CREB, and glial fibrillary acidic protein. Intraventricular injection of K252a, a tyrosine kinase B receptor antagonist, markedly reduced SB‐induced cell proliferation detected by BrdU and Ki67 in the ipsilateral SVZ, DG, and other brain regions, blocked SB‐induced nestin expression and CREB activation, and attenuated the long‐lasting behavioral benefits of SB. Together, these results suggest that histone deacetylase inhibitor‐induced cell proliferation, migration and differentiation require BDNF–tyrosine kinase B signaling and may contribute to long‐term beneficial effects of SB after ischemic injury.
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Sodium butyrate stimulates BDNF expression, neurogenesis, and neural proliferation in rodents and facilitates long-term memory consolidation.
“BDNF expression, neurogenesis, and neural proliferation in rodents (124–126), as well as facilitation of long-term memory consolidation, were stimulated by sodium butyrate (127).”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [124]
Citation 127 is attached to the claim about long-term memory consolidation, not the preceding BDNF and neurogenesis claims. The Results section on long-term behavioral benefits reports improved rotarod and motor, sensory, and reflex performance after ischemia, but does not address memory consolidation. Searches for “long-term memory consolidation” and memory-related outcomes found no supporting passage in our copy. (LLM, conf=0.76)
Experimental — accuracy not yet measuredHDAC inhibition enhances long-term potentiation and contextual fear memory.
“These studies have reported an enhancement of long-term potentiation (LTP) and contextual fear memory induced by HDAC inhibition (124, 127, 136, 137), pointing out enteric SCFAs as a promising learning and memory modulators.”
From The Role of Short-Chain Fatty Acids From Gut Microbiota in Gut-Brain Communication (2020) · cites this paper as [124]
The Results section on long-term behavioral benefits reports improved motor, sensory, and reflex performance after sodium butyrate treatment in ischemic rats, not long-term potentiation or contextual fear memory. Searches for those terms and for learning, memory, and fear conditioning found no passage in our copy addressing the attributed claim; page numbers were not provided. (LLM, conf=0.76)
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- Authors
- Kim, H. J., Leeds, P., & Chuang, D.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Chuang, De‐Maw
- ORCID
- Kim, Hyeon Ju
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2009-07-21
- Volume
- 110
- Issue
- 4
- Pages
- 1226-1240
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- PMC
- PMC2726719
- OpenAlex
- W1493226253
- Cited by
- 332
- References
- 51
- Citations by year
- 2026: 14 · 2025: 20 · 2024: 17 · 2023: 16 · 2022: 34 · 2021: 11 · 2020: 24 · 2019: 22 · 2018: 21 · 2017: 18 · 2016: 23 · 2015: 22 · 2014: 23 · 2013: 15 · 2012: 18
- FWCI
- 5.44
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Mental Health (Z01MH002468)
- Topics
- Life Sciences › Neuroscience › Developmental Neuroscience › Neurogenesis and neuroplasticity mechanisms
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Neurology › Neurological Disease Mechanisms and Treatments
- Keywords
- sodium butyrate, histone deacetylase inhibitors, neurogenesis, cerebral ischemia, subventricular zone, dentate gyrus, brain-derived neurotrophic factor, TrkB receptor, CREB, nestin, polysialic acid, glial fibrillary acidic protein, cell proliferation, cell migration, cell differentiation, stroke recovery
- MeSH terms
- Animals, Brain, Bromodeoxyuridine, Butyrates, Cell Differentiation, Brain Ischemia, Disease Models, Animal, Enzyme Inhibitors, Histone Deacetylases, Intermediate Filament Proteins, Male, Nerve Regeneration, Nerve Tissue Proteins, Sialic Acids, Biomarkers, Rats, Sprague-Dawley, Cyclic AMP Response Element-Binding Protein, Brain-Derived Neurotrophic Factor, Brain Infarction, Receptor, trkB, Neural Cell Adhesion Molecule L1, Cell Proliferation, Rats, Neurogenesis, Histone Deacetylase 1, Histone Deacetylase Inhibitors, Nestin
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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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