ArticleRestorative neurology and neuroscience2008
TrkB gene transfer does not alter hippocampal neuronal loss and cognitive deficits following traumatic brain injury in mice.
Article in Restorative neurology and neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Lower and higher volumes of physical exercise build up brain reserves against memory deficits triggered by a head injury in mice.Experimental neurology · 2023Article
- Altering the Trajectory of Perfusion-Diffusion Deficits Using A BDNF Mimetic Acutely After TBI is Associated with Improved Functional Connectivity.Progress in neurobiology (Dover, Del.) · 2023Article
- Neuron-Targeted Caveolin-1 Improves Molecular Signaling, Plasticity, and Behavior Dependent on the Hippocampus in Adult and Aged Mice.Biological psychiatry · 2017Article
- Effects of AAV-mediated knockdown of nNOS and GPx-1 gene expression in rat hippocampus after traumatic brain injury.PloS one · 2017Article
- Membrane lipid rafts and neurobiology: age-related changes in membrane lipids and loss of neuronal function.The Journal of physiology · 2016Review
- The Small-Molecule TrkB Agonist 7, 8-Dihydroxyflavone Decreases Hippocampal Newborn Neuron Death After Traumatic Brain Injury.Journal of neuropathology and experimental neurology · 2015Article
- Traumatic brain injury enhances neuroinflammation and lesion volume in caveolin deficient mice.Journal of neuroinflammation · 2014Article
- Inflammatory consequences in a rodent model of mild traumatic brain injury.Journal of neurotrauma · 2013Article
- Calpastatin overexpression protects axonal transport in an in vivo model of traumatic axonal injury.Journal of neurotrauma · 2012Article
- Small molecule BDNF mimetics activate TrkB signaling and prevent neuronal degeneration in rodents.The Journal of clinical investigation · 2010Article
- Exercise-induced improvement in cognitive performance after traumatic brain injury in rats is dependent on BDNF activation.Brain research · 2009Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
purposeThe ability of brain-derived neurotrophic factor (BDNF) to attenuate secondary damage and influence behavioral outcome after experimental traumatic brain injury (TBI) remains controversial. Because TBI can result in decreased expression of the trkB receptor, thereby preventing BDNF from exerting potential neuroprotective effects, the contribution of both BDNF and its receptor trkB to hippocampal neuronal loss and cognitive dysfunction were evaluated.
methodsFull-length trkB was overexpressed in the left hippocampus of adult C57Bl/6 mice using recombinant adeno-associated virus serotype 2/5 (rAAV 2/5). EGFP (enhanced green fluorescent protein) expression was present at two weeks after AAV-EGFP injection and remained sustained up to four weeks after the injection. At 2 weeks following gene transduction, mice were subjected to parasagittal controlled cortical impact (CCI) brain injury, followed by either BDNF or PBS infusion into the hippocampus.
resultsNo differences were observed in learning ability at two weeks post-injury or in motor function from 48 hours to two weeks among treatment groups. The number of surviving pyramidal neurons in the CA2-CA3 region of the hippocampus was also not different among treatment groups.
conclusionsThese data suggest that neither overexpression of trkB, BNDF infusion or their combination affects neuronal survival or behavioral outcome following experimental TBI in mice.
Indexed as
Identifiers
18431005PMC2580053W1569086356What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.