Noggin Bonks and Neurogenesis: Alterations in Neurogenesis and Gliogenesis Following a Rodent Model of Traumatic Brain Injury (TBI)

Author

• Tuesday Kirby Kahl, Portland State University, Oregon Health & Science UniversityFollow
• Priscilla Ambrosi, Oregon Health & Science University
• Corwin Butler, Oregon Health & Science University
• Elizabeth Moss, Oregon Health & Science UniversityFollow

First Advisor

Elizabeth Moss

Date of Award

Spring 6-2026

Document Type

Thesis

Degree Name

Bachelor of Science (B.S.) in Psychology and University Honors

Department

Psychology

Language

English

Subjects

neurogenesis, gliogenesis, granule cells, olfactory bulb, astrocytes, neurons

Abstract

Traumatic Brain Injuries (TBIs) produce a variety of symptoms and complications in humans including epilepsy, mood changes and alterations in sensory perception. Neurogenesis, the proliferation of new neurons, following a TBI, is well-documented. While brain damage and subsequent neurogenesis and gliogenesis can vary based on location and severity of a TBI, we know that post-injury inflammation is driving most of the glial response. However, the post-injury timeline and the shift in cell phenotypes over time is lesser known. We aimed to quantify gliogenesis and neurogenesis rates during the post-acute recovery phase following TBI, determine the source of these migrating adult-born cells, their resulting phenotypes and characterize their morphology in destination circuits. To visualize proliferating cells after injury, we used a Controlled Cortical Impact (CCI) model followed by cell proliferation tracking using BrdU labeling at seven days post-injury. We found increases in BrdU density on the ipsilateral side of the brain in the thalamus, cortex and hippocampus, with no significant changes in the olfactory bulb (OB). To determine whether proliferating cells originated in the Subventricular Zone (SVZ), we injected lentiviruses expressing fluorescent markers into the SVZ followed by CCI, Sham or no surgery. We observed no labeled somas outside of the SVZ and OB, demonstrating that neural progenitors weren’t being diverted from the SVZ post-TBI. To determine whether adult-born granule cells that reached the OB post-TBI were typical or abnormal, we quantified the morphology of lentivirus-labeled adult born cells using Scholl’s analysis and found that in CCI mice, these cells possessed less apical dendrite complexity. These findings highlight the whole brain and hemispheric implications following TBI and highlight the challenges for new cells to migrate and integrate into the post-injury environment.

Recommended Citation

Kahl, Tuesday Kirby; Ambrosi, Priscilla; Butler, Corwin; and Moss, Elizabeth, "Noggin Bonks and Neurogenesis: Alterations in Neurogenesis and Gliogenesis Following a Rodent Model of Traumatic Brain Injury (TBI)" (2026). University Honors Theses. Paper 1872.