Neuroscience, 2009-09, Vol.163 (1), p.1-8
2009
Details
- Autor(en) / Beteiligte
- Titel
- Histone deactylase inhibition combined with behavioral therapy enhances learning and memory following traumatic brain injury
- Ist Teil von
- Neuroscience, 2009-09, Vol.163 (1), p.1-8
- Ort / Verlag
- Amsterdam: Elsevier Ltd
- Erscheinungsjahr
- 2009
- Link zum Volltext
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Abstract Traumatic brain injury (TBI) induces a number of pathological events ranging from neuronal degeneration and tissue loss to impaired neuronal plasticity and neurochemical dysregulation. In rodents, exposure of brain-injured animals to environmental enrichment has been shown to be an effective means of enhancing learning and memory post-injury. Recently, it has been discovered that environmental enrichment may enhance neuronal plasticity through epigenetic changes that involve enhanced histone acetylation, a property that can be mimicked by the use of histone deactylase (HDAC) inhibitors. We therefore evaluated the consequences of the HDAC inhibitor sodium butyrate on the learning and memory of brain-injured mice. In contrast to a previous report using a mouse neurodegeneration model, sodium butyrate (1.2 g/kg daily for four weeks) did not improve learning and memory when tested after the completion of the drug treatment paradigm. In addition, sodium butyrate administration during the reported period of neurodegeneration (days 0–5) also offered no benefit. However, when administered concurrently with training in the Morris water maze task (beginning on day 14 post-injury), sodium butyrate improved learning and memory in brain-injured mice. Interestingly, when these mice were subsequently tested in an associative fear conditioning task, an improvement was observed. Taken together, our findings indicate that HDAC inhibition may mimic some of the cognitive improvements seen following enriched environment exposure, and that the improvement is observed when the treatment is carried out current with behavioral testing.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0306-4522eISSN: 1873-7544DOI: 10.1016/j.neuroscience.2009.06.028Titel-ID: cdi_proquest_miscellaneous_20705131
- Format
- –
- Schlagworte
- Animals, Avoidance Learning - drug effects, Avoidance Learning - physiology, Behavior Therapy - methods, Biological and medical sciences, Brain - drug effects, Brain - enzymology, Brain - physiopathology, Brain Injuries - drug therapy, Brain Injuries - enzymology, Brain Injuries - genetics, Butyrates - pharmacology, Butyrates - therapeutic use, Conditioning (Psychology) - drug effects, Conditioning (Psychology) - physiology, delay fear conditioning, Disease Models, Animal, Environment, Controlled, Epigenesis, Genetic - drug effects, Epigenesis, Genetic - genetics, Fundamental and applied biological sciences. Psychology, HDAC, hippocampus, Histone Deacetylase 1 - antagonists & inhibitors, Histone Deacetylase 1 - genetics, Histone Deacetylase 1 - metabolism, Injuries of the nervous system and the skull. Diseases due to physical agents, Learning Disorders - drug therapy, Learning Disorders - enzymology, Learning Disorders - genetics, Male, Maze Learning - drug effects, Maze Learning - physiology, Medical sciences, Memory Disorders - drug therapy, Memory Disorders - enzymology, Memory Disorders - genetics, Mice, Mice, Inbred C57BL, Morris water maze, Nerve Degeneration - drug therapy, Nerve Degeneration - enzymology, Nerve Degeneration - genetics, Neurology, Neuronal Plasticity - genetics, Physical Stimulation, Traumas. Diseases due to physical agents, traumatic brain injury, Vertebrates: nervous system and sense organs