Neuroscience 2005 Abstract
| Presentation Number: | 334.3 |
|---|---|
| Abstract Title: | Development and implementation of a controlled cortical impact model of traumatic brain injury: characterization based on MRI, histology and behavioral data. |
| Authors: |
Onyszchuk, G.*1,3
; He, Y.3
; Al-Hafez, B.3
; Bilgen, M.1,3
; Berman, N. E. J.2
; Brooks, W. M.1,3
1Molecular & Integrative Physiology, Univ. of Kansas Med. Ctr., Kansas City, KS 2Anatomy & Cell Biology, Univ. of Kansas Med. Ctr., Kansas City, KS 3Hoglund Brain Imaging Center, Univ. of Kansas Med. Ctr., Kansas City, KS |
| Primary Theme and Topics |
Disorders of the Nervous System - Trauma -- Brain: Animal models and human studies |
| Session: |
334. Brain Trauma: Animal Models and Human Studies I Poster |
| Presentation Time: | Sunday, November 13, 2005 3:00 PM-4:00 PM |
| Location: | Washington Convention Center - Hall A-C, Board # UU75 |
| Keywords: | TBI, CCI, Magnetic Resonance Imaging, Edema |
Traumatic brain injury (TBI) is the leading cause of death and disability in children and young adolescents in the United States. Animal models of reproducible TBI are necessary to characterize the mechanisms involved in damage and repair at the tissue, cellular and molecular levels. We established a mouse model of TBI, using a computer-driven, controlled cortical impact (CCI) device, and a stereotactic head holder. The CCI device is based on a microprocessor-controlled linear motor, where strike velocity, contusion depth and contusion time are precisely controlled and monitored through a real-time interface.
Using high field strength (9.4T) magnetic resonance imaging (MRI), we obtained longitudinal data by scanning mice at 24 hours, 72 hours, 7 and 14 days after injury. We used behavioral assessments and traditional histological techniques to validate the model. MRI has also been used to validate injury severity and location, enabling efficient optimization of the model and CCI device parameters.
Our results indicate that our model can deliver an injury with high reproducibility and high adjustability. Lesion volume data, obtained from both axial and sagittal T2-weighted MRI spin-echo images taken 14 days after injury, for an moderately-injured initial animal group (n=8), demonstrate the lesion consistency: mean lesion volume is 6.9 cubic millimeters (std. error = 0.28). Sensorimotor deficits for the same animal group, as measured by Rotarod, are greatest at 48 hours post injury, where mean 18rpm latency = 42% of pre-injury performance (std. error = 6%), and recover to 88% of pre-injury performance (std. error = 13%) by 14 days post injury. With this model now established, we plan to use it to answer basic questions about the role of edema, inflammation and apoptosis in primary and secondary damage and repair in traumatic brain injury.
Using high field strength (9.4T) magnetic resonance imaging (MRI), we obtained longitudinal data by scanning mice at 24 hours, 72 hours, 7 and 14 days after injury. We used behavioral assessments and traditional histological techniques to validate the model. MRI has also been used to validate injury severity and location, enabling efficient optimization of the model and CCI device parameters.
Our results indicate that our model can deliver an injury with high reproducibility and high adjustability. Lesion volume data, obtained from both axial and sagittal T2-weighted MRI spin-echo images taken 14 days after injury, for an moderately-injured initial animal group (n=8), demonstrate the lesion consistency: mean lesion volume is 6.9 cubic millimeters (std. error = 0.28). Sensorimotor deficits for the same animal group, as measured by Rotarod, are greatest at 48 hours post injury, where mean 18rpm latency = 42% of pre-injury performance (std. error = 6%), and recover to 88% of pre-injury performance (std. error = 13%) by 14 days post injury. With this model now established, we plan to use it to answer basic questions about the role of edema, inflammation and apoptosis in primary and secondary damage and repair in traumatic brain injury.
Supported by NS039123-04
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2005 Neuroscience Meeting Planner. Washington, DC: Society for Neuroscience, 2005. Online.
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