Presentation Details
| Noggin Bonks and Neurogenesis: Alterations in Olfactory Bulb Adult Neurogenesis Following a Mouse Model of TBI Tuesday Kirby Kahl1, 2, Priscilla Ambrosi1, Cory Butler1, Elizabeth Moss1. 1Oregon Health Sciences University, Portland, OR, USA.2Portland State University, Portland, OR, USA |
Abstract
Traumatic Brain Injuries (TBIs) produce a variety of symptoms and complications in humans and often result in extensive cell death in the brain. In adulthood, neurogenesis, predominantly occurs in the Hippocampus and Subventricular Zone (SVZ). SVZ neural progenitors migrate along the Rostral Migration Stream (RMS) to the Olfactory Bulb (OB) where they become interneurons. Following TBI, there is a spike in neurogenesis in the hippocampus but little is known about the impacts to olfactory bulb neurogenesis. To investigate the location of adult born cells following a TBI, we used a controlled cortical impact (CCI) mouse model of TBI followed by cell proliferation tracking using BrdU pulse labeling at 7-10 days post-injury. We also found surprising increases in adult-born cells on the ipsilateral side of the brain, particularly near the injury site, in the peri-infarct cortex, dentate gyrus and ipsilateral thalamus. immunohistochemistry revealed an astrocytic phenotype of most newborn cells. At the same time, we found a decrease in adult-born neurons in the OB. To determine whether neurons that successfully reach the OB were typical or abnormal as a result of being born and migrating under pathological and inflammatory conditions, we injected Lentivirus into the SVZ followed by CCI, Sham surgery or no surgery. This demonstrated that neural progenitors were not being diverted from the SVZ. Furthermore, lentivirus labeled adult born neurons in the OB of CCI mice appeared qualitatively morphologically abnormal, with less complex arbors. This appears true of mature neurons, no longer expressing DCX, an immature neuronal marker, and of immature viral labeled cells colabeled with DCX.
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