Abstract
Time course of changes in neuroinflammatory processes in the dorsal and ventral hippocampus was studied during the early period after lateral fluid percussion-induced neocortical traumatic brain injury (TBI) in the ipsilateral and contralateral hemispheres. In the ipsilateral hippocampus, neuroinflammation (increase in expression of pro-inflammatory cytokines) was evident from day 1 after TBI and ceased by day 14, while in the contralateral hippocampus, it was mainly limited to the dorsal part on day 1. TBI induced an increase in hippocampal corticosterone level on day 3 bilaterally and an accumulation of Il1b on day 1 in the ipsilateral hippocampus. Activation of microglia was observed from day 7 in different hippocampal areas of both hemispheres. Neuronal cell loss was detected in the ipsilateral dentate gyrus on day 3 and extended to the contralateral hippocampus by day 7 after TBI. The data suggest that TBI results in distant hippocampal damage (delayed neurodegeneration in the dentate gyrus and microglia proliferation in both the ipsilateral and contralateral hippocampus), the time course of this damage being different from that of the neuroinflammatory response.
Highlights
A leading cause of disability among young people is traumatic brain injury (TBI), a damage to the brain that occurs as a result of exposure to external mechanical force [1, 2, 3]
We investigated the time course of changes in the levels of gene expression associated with the neuroinflammation and stress reactivity in the dorsal and ventral hippocampus, corticosterone and proinflammatory cytokines concentrations in the dorsal and ventral hippocampus and blood serum, as well as the hippocampal microglia state during early period after TBI
We found that lateral fluid percussion-induced TBI altered the tissue morphology in the dentate gyrus (DG), CA1 and CA3 areas of the hippocampus
Summary
A leading cause of disability among young people is traumatic brain injury (TBI), a damage to the brain that occurs as a result of exposure to external mechanical force [1, 2, 3]. TBI can result in temporary or permanent impairments of cognitive and motor functions as well as the development of other neurological complications [1, 4]. Regardless of the injury severity, the delayed period after TBI in lots of patients is associated with the development of comorbid cognitive disorders, down to dementia, as well as emotional disturbances, commonly depression [6], which are believed to be associated with the dysfunction of the hippocampus. Deeper structures, including the hippocampus, are not directly damaged at the moment of injury, and their delayed damage is distant, relative to the region of primary damage. The TBI-induced distant damage may involve the ipsilateral, and the contralateral hippocampus (see [6, 7] for review)
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