ArticleFrontiers in cellular neuroscience2013
Impact of trichostatin A and sodium valproate treatment on post-stroke neurogenesis and behavioral outcomes in immature mice.
Article in Frontiers in cellular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Epigenetic mechanisms in aneurysm formation, growth, and rupture: A systematic review.Interventional neuroradiology : journal of peritherapeutic neuroradiology, surgical procedures and related neurosciences · 2025Review
- Ischemic Stroke and the Biological Hallmarks of Aging.Aging and disease · 2024Review
- Transient plasticity response is regulated by histone deacetylase inhibitor in oxygen-glucose deprivation condition.Pharmacological reports : PR · 2023Article
- Negative regulation of angiogenesis and the MAPK pathway may be a shared biological pathway between IS and epilepsy.PloS one · 2023Article
- Epigenetic mechanisms and potential therapeutic targets in stroke.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2022Review
- Therapeutic effectiveness of a single exercise session combined with WalkAide functional electrical stimulation in post-stroke patients: a crossover design study.Neural regeneration research · 2021Article
- Impact of a Histone Deacetylase Inhibitor-Trichostatin A on Neurogenesis after Hypoxia-Ischemia in Immature Rats.International journal of molecular sciences · 2020Article
- Effect of the HDAC Inhibitor, Sodium Butyrate, on Neurogenesis in a Rat Model of Neonatal Hypoxia-Ischemia: Potential Mechanism of Action.Molecular neurobiology · 2019Article
- Epigenetic regulation of inflammation in stroke.Therapeutic advances in neurological disorders · 2018Review
- Sodium Butyrate, a Histone Deacetylase Inhibitor, Exhibits Neuroprotective/Neurogenic Effects in a Rat Model of Neonatal Hypoxia-Ischemia.Molecular neurobiology · 2017Article
- The potential neuroprotective role of a histone deacetylase inhibitor, sodium butyrate, after neonatal hypoxia-ischemia.Journal of neuroinflammation · 2017Article
- Epigenetic mechanisms of neuroplasticity and the implications for stroke recovery.Experimental neurology · 2015Review
- The role of inflammation in perinatal brain injury.Nature reviews. Neurology · 2015Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Stroke in the neonatal brain frequently results in neurologic impairments including cognitive disability. We investigated the effect of long-term sodium valproate (valproate) and trichostatin A (TSA) treatment upon post-stroke neurogenesis in the dentate gyrus (DG) of stroke-injured immature mice. Decreased or abnormal integration of newborn DG neurons into hippocampal circuits can result in impaired visual-spatial function, abnormal modulation of mood-related behaviors, and the development of post-stroke epilepsy. Unilateral carotid ligation of P12 CD1 mice was followed by treatment with valproate, TSA, or vehicle for 2 weeks, bromodeoxyuridine (BrdU) administration for measurement of neurogenesis, and perfusion at P42 or P60. Behavior testing was conducted from P38-42. No detrimental effects on behavior testing were noted with TSA treatment, but mildly impaired cognitive function was noted with valproate-treated injured animals compared to normal animals. Significant increases in DG neurogenesis with both TSA and valproate treatment were noted with later administration of BrdU. Increased mortality and impaired weight gain was noted in the valproate-treated ligated animals, but not in the TSA-treated animals. In summary, the impact of histone deacetylase (HDAC) inhibition upon post-stroke subgranular zone neurogenesis is likely to depend on the age of the animal at the time point when neurogenesis is assessed, duration of HDAC inhibition before BrdU labeling, and/or the stage in the evolution of the injury.
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Registered trials
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