title: Diffusion tensor imaging of hippocampal network plasticity.
abstract: Diffusion tensor imaging (DTI) has become a valuable tool to investigate white matter integrity in the brain. DTI also gives contrast in gray matter, which has been relatively little explored in studies assessing post-injury structural abnormalities. The present study was designed to compare white and gray matter reorganization in the rat hippocampus after two epileptogenic brain injuries, status epilepticus (SE) and traumatic brain injury (TBI), using ex vivo high-resolution DTI. Imaging was performed at 6-12 months post-injury and findings were compared to histological analyses of Nissl, myelin, and Timm-stained preparations from the same animals. In agreement with the severity of histological damage, fractional anisotropy (FA), axial (D ||) and radial (D ⊥) diffusivities, and mean diffusivity (MD) measurements were altered in the order SE > TBI ipsilaterally > TBI contralaterally. After SE, the most severe abnormalities were found in the dentate gyrus and CA3b-c subfields, in which the mean FA was increased to 125 % (p < 0.001) and 143 % (p < 0.001) of that in controls, respectively. In both subfields, the change in FA was associated with an increase in D || (p < 0.01). In the stratum radiatum of the CA1, FA was decreased to 81 % of that in controls (p < 0.05) which was associated with an increase in D ⊥ (p < 0.01). After TBI, DTI did not reveal any major abnormalities in the dentate gyrus. In the ipsilateral CA3b-c, however, FA was increased to 126 % of that in controls (p < 0.01) and associated with a mild decrease in D ⊥ (p < 0.05). In the stratum radiatum of the ipsilateral CA1, FA was decreased to 88 % of that in controls (p < 0.05). Our data demonstrate that DTI reveals subfield-specific abnormalities in the hippocampus with remarkable qualitative and quantitative differences between the two epileptogenic etiologies, suggesting that DTI could be a valuable tool for follow-up of focal circuitry reorganization during the post-injury aftermath.
authors.affiliation: Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, PO Box 1627, 70211, Kuopio, Finland.
authors.forename: Alejandra
authors.initials: A
authors.lastname: Sierra
authors.forename: Teemu
authors.initials: T
authors.lastname: Laitinen
authors.forename: Olli
authors.initials: O
authors.lastname: Gröhn
authors.forename: Asla
authors.initials: A
authors.lastname: Pitkänen
mesh_terms: D000818:Animals; D001930:Brain Injuries / Q000473:pathology*; D056324:Diffusion Tensor Imaging; D066128:Gray Matter / Q000473:pathology*; D006624:Hippocampus / Q000473:pathology*; D008297:Male; D009415:Nerve Net / Q000473:pathology; D009473:Neuronal Plasticity; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D013226:Status Epilepticus / Q000473:pathology*; D066127:White Matter / Q000473:pathology*