No real clue on what this means so go ask your researcher or
great stroke association.
http://www.frontiersin.org/cellular_neuroscience/10.3389/fncel.2013.00123/full?
Shanu George1,
Shilpa D. Kadam1,2,3,
Natasha D. Irving1,
Geoffrey J. Markowitz1,
Saba Raja1,
Anthony Kwan1, YuShan Tu
1, Huigen Chen
1, Charles Rohde
4, Dani R. Smith
5 and
Anne M. Comi1,3,6*
- 1Department of Neurology and Developmental Medicine, Hugo Moser Kennedy Krieger Research Institute, Baltimore, MD, USA
- 2Neuroscience, Kennedy Krieger Institute, Baltimore, MD, USA
- 3Department of Neurology, Johns Hopkins School of Medicine, Baltimore, MD, USA
- 4Department of Biostatistics, Johns Hopkins School of Public Health, Baltimore, MD, USA
- 5Neurogenetics and Behavior Center, Department of Psychological and Brain Sciences, Johns Hopkins University, Baltimore, MD, USA
- 6Department of Pediatrics, Johns Hopkins School of Medicine, Baltimore, MD, USA
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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