Spinal cord injury (SCI) is a traumatic event with devastating consequences for the physical and mental condition of patients. There is increasing evidence that SCI affects not only motor functions, but also sensory and autonomic functions and thus reduces quality of life of people living with the injury. SCI is also associated with loss of smell and changes in the brain neural circuity, so it is important to determine the relationship between spinal cord injury and the olfactory function. The first goal of the study was to use intranasal administration of wheat germ agglutinin conjugated to horseradish peroxidase (WGA-HRP) to trace sensory neurons of the olfactory tract from the nasal olfactory epithelium to the olfactory bulb in the rat brain. The WGA-HRP tracing was compared between healthy rats and rats with spinal cord injury. In addition to WGA-HRP tracing, the goal of the study was to examine the pattern and intesity of glutamic acid decarboxylase (GAD67) immunofluorescence, neural nuclei (NeuN) staining as well as activation of microglia. Immunohistochemical staining methods were performed on sagittal and coronal sections of the olfactory bulbs harvested from healthy rats and those with spinal cord injury. The results were finally analyzed using a fluorescent microscope. Fluorescence intensity of WGA-HRP tracer, GAD67 and microglia was compared between healthy and SCI rats. The data showed that there are differences in WGA- HRP signal intensity between SCI and control animals, with the signal being weaker after the injury. There are also differences in the GAD67 signal, with it being stronger following SCI. Microglia also emitted more fluorescence after SCI with their morphology shifted from inactive to an active state. These data indicate changes in olfactory architecture following SCI. The transmission of nerve stimuli from olfactory epithelium through the olfactory bulb to the brain is reduced, and microglial activation triggers inflammatory processes by secreting cytokines within the olfactory bulb.