| Autor: |
Yu F; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 2 Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences , Bethesda, Maryland., Shukla DK; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 5 Department of Psychiatry, University of Maryland School of Medicine , Baltimore, Maryland., Armstrong RC; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 2 Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 3 Program in Neuroscience, Uniformed Services University of the Health Sciences , Bethesda, Maryland., Marion CM; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 3 Program in Neuroscience, Uniformed Services University of the Health Sciences , Bethesda, Maryland., Radomski KL; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 2 Department of Anatomy, Physiology and Genetics, Uniformed Services University of the Health Sciences , Bethesda, Maryland., Selwyn RG; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 6 Department of Radiology, University of New Mexico , Albuquerque, New Mexico ., Dardzinski BJ; 1 Center for Neuroscience and Regenerative Medicine, Uniformed Services University of the Health Sciences , Bethesda, Maryland.; 4 Department of Radiology and Radiological Sciences, Uniformed Services University of the Health Sciences , Bethesda, Maryland. |
| Abstrakt: |
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 (K a ) 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. |
