TBI stands for Traumatic Brain Injury and refers to damage to the brain resulting from an external physical force, such as a blow, jolt, or penetrating injury to the head. Common causes of TBI include falls, motor vehicle accidents, sports injuries, and violence and has been linked to thousands of deaths and injuries in the US and the EU alike. This thesis was aimed to localise certain TBI to a specific part of the brain by exerting similar loading conditions on an Finite Element Method (FEM) of the rat brain as physical experiments conducted on living rats. By comparing the strain in 7 vital parts of the brain to injury diagnosis conducted in the physical experiments, an effort was made to link localised strain to injury diagnosis. The results indicate that strain in the thalamus and hypothalamus are linked with a loss of consciousness while strain in the hypothalamus coupled with the neocortex correlates greatly with activity-based behaviour changes. Lastly, injury associated with emotional changes are believed to stem from large strains in the neocortex. There is a theory suggesting that the structure of myeline, which provides support in motion and movement patterns of biological systems in humans and animals (known as biomechanical kinematics), could have an impact. However, more studies are needed to confirm and determine the exact cause. / TBI, från engelskans Traumatic Brain Injury, står för Traumatisk Hjärn Skada och syftar på en skada i hjärnan till följd av enyttre fysisk kraft, såsom ett slag, stöt eller genomträngande skada i huvudet. Vanliga orsaker till TBI inkluderar fall, motorfordonsolyckor, sportskador och våld och har kopplats till tusentals dödsfall och skadade i både USA och EU. Denna rapport syftar till att försöka lokalisera viss TBI till en specifik del av hjärnan genom att utöva liknandebelastningsförhållanden på en finit elementmetod (FEM) modell av råtthjärnan som fysiska experimentutförs på levande råttor. Genom att jämföra belastningen i 7 vitala delar av hjärnan med skadediagnos som utfördes i de fysiska experimenten gjordes en ansträngning för att koppla lokaliserad belastning till skadediagnos. Resultaten indikerar att skada i thalamus och hypotalamus är kopplade till en förlust av medvetande medan belastning i hypotalamus i kombination med neocortex korrelerar kraftigtmed aktivitetsbaserade beteendeförändringar. Slutligen är skador i samband med känslomässiga förändringartros härröra från skada i neocortex. Det finns teori som tyder på attstruktur av myelin, som ger stöd i rörelse och rörelsemönster av biologiskasystem hos människor och djur (känd som biomekanisk kinematik), kan ha en inverkan.Det behövs dock fler studier för att bekräfta och fastställa den exakta orsaken.

Stress has been reported to activate the locus coeruleus (LC)-noradrenergic system. In this study, corticosterone (CORT) was orally administrated to rats for 21 days to mimic stress status. In situ hybridization measurements showed that CORT ingestion significantly increased mRNA levels of norepinephrine transporter (NET) and dopamine β-hydroxylase (DBH) in the LC region. Immunofluorescence staining and western blotting revealed that CORT treatment also increased protein levels of NET and DBH in the LC, as well as NET protein levels in the hippocampus, the frontal cortex and the amygdala. However, CORT-induced increase in DBH protein levels only appeared in the hippocampus and the amygdala. Elevated NET and DBH expression in most of these areas (except for NET protein levels in the LC) was abolished by simultaneous treatment with combination of corticosteroid receptor antagonist mifepristone and spironolactone (s.c. for 21 days). Also, treatment with mifepristone alone prevented CORT-induced increases of NET expression and DBH protein levels in the LC. In addition, behavioral tasks showed that CORT ingestion facilitated escape in avoidance trials using an elevated T-maze, but interestingly, there was no significant effect on the escape trial. Corticosteroid receptor antagonists failed to counteract this response in CORT-treated rats. In the open-field task, CORT treatment resulted in less activity in a defined central zone compared to controls and corticosteroid receptor antagonist treatment alleviated this increase. In conclusion, this study demonstrates that chronic exposure to CORT results in a phenotype that mimics stress-induced alteration of noradrenergic phenotypes, but the effects on behavior are task dependent. As the sucrose consumption test strongly suggests CORT ingestion-induced depression-like behavior, further elucidation of underlying mechanisms may improve our understanding of the correlation between stress and the development of depression.