Repetitive Model of Mild Traumatic Brain Injury Produces Cortical Abnormalities Detectable by Magnetic Resonance Diffusion Imaging, Histopathology, and Behavior
| Autor: | Fengshan Yu, Dinesh K Shukla, Reed Selwyn, Kryslaine L. Radomski, Regina C. Armstrong, Christina M. Marion, Bernard J. Dardzinski |
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| Rok vydání: | 2017 |
| Předmět: |
Male
0301 basic medicine diffusion kurtosis imaging Pathology medicine.medical_specialty Traumatic brain injury microglia Poison control Corpus callosum Corpus Callosum Mice 03 medical and health sciences 0302 clinical medicine Thy1-YFP Fractional anisotropy Concussion Animals Medicine Diffusion Kurtosis Imaging Brain Concussion Cerebral Cortex Behavior Animal medicine.diagnostic_test business.industry Magnetic resonance imaging Original Articles diffusion tensor imaging medicine.disease Axons Mice Inbred C57BL Disease Models Animal Diffusion Magnetic Resonance Imaging 030104 developmental biology nervous system concussion Neurology (clinical) business 030217 neurology & neurosurgery Diffusion MRI |
| Zdroj: | Journal of Neurotrauma |
| ISSN: | 1557-9042 0897-7151 |
| DOI: | 10.1089/neu.2016.4569 |
| Popis: | Noninvasive detection of mild traumatic brain injury (mTBI) is important for evaluating acute through chronic effects of head injuries, particularly after repetitive impacts. To better detect abnormalities from mTBI, we performed longitudinal studies (baseline, 3, 6, and 42 days) using magnetic resonance diffusion tensor imaging (DTI) and diffusion kurtosis imaging (DKI) in adult mice after repetitive mTBI (r-mTBI; daily × 5) or sham procedure. This r-mTBI produced righting reflex delay and was first characterized in the corpus callosum to demonstrate low levels of axon damage, astrogliosis, and microglial activation, without microhemorrhages. High-resolution DTI-DKI was then combined with post-imaging pathological validation along with behavioral assessments targeted for the impact regions. In the corpus callosum, only DTI fractional anisotropy at 42 days showed significant change post-injury. Conversely, cortical regions under the impact site (M1–M2, anterior cingulate) had reduced axial diffusivity (AD) at all time points with a corresponding increase in axial kurtosis (Ka) at 6 days. Post-imaging neuropathology showed microglial activation in both the corpus callosum and cortex at 42 days after r-mTBI. Increased cortical microglial activation correlated with decreased cortical AD after r-mTBI (r = −0.853; n = 5). Using Thy1-YFP-16 mice to fluorescently label neuronal cell bodies and processes revealed low levels of axon damage in the cortex after r-mTBI. Finally, r-mTBI produced social deficits consistent with the function of this anterior cingulate region of cortex. Overall, vulnerability of cortical regions is demonstrated after mild repetitive injury, with underlying differences of DTI and DKI, microglial activation, and behavioral deficits. |
| Databáze: | OpenAIRE |
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