Thalamus is the brain region whose damage has been well documented after both human and experimental traumatic brain injury (TBI). Molecular mechanisms which lead to posttraumatic cell death or support the neuronal survival in the thalamus, in this entity, have not yet been fully characterized. Therefore, aim of this study was to determine the changes in several markers of inflammation and also cell protection following experimental TBI in the rat. Experiments were carried out on adult male rats. TBI of moderate severity was performed over the left parietal cortex using the lateral fiuid percussion brain injury model. Sham-operated animals were used as the control group. Rats were sacrificed 24 h after the TBI induction and the thalami were processed for the Western blot analyses of different protein expressions. TBI caused significant increases of the cyclooxygenase-2, inducible nitric oxide synthase and heat shock protein 70 expressions in the thalamus of rats with TBI in relation to the values registered in sham-operated animals. Thalamic expressions of inhibitory kappa B alpha and brain derived neurotrophic factor were unaffected by TBI in our experimental conditions.