Inflammatory pain occurs as a result of inflammation or tissue mJury which causes the secretion of various inflammatory mediators that act directly by activating nociceptors or interfere with the signaling processes inside them. Frequent outbreak of primary neurons leads to numerous changes in CNS accompanied by phenomena such as sensitization, hyperalgesia and allodynia. Numerous studies have shown the important role of endogenous opioid system in the process of transmission and modulation of painful information. Out of three main groups of opioid peptides, most evidence of involvement in nociceptive processes in the spinal level is available for enkephalins. Opioid analgesics have long found a place in clinical practice. Recent research studies potential of their use in chronic diseases, among which are inflammatory diseases like rheumatoid arthritis or osteoarthritis. This thesis is based on measurment of enkephalin immunoreactivity in tissue samples of dorsal hom of the spinal cord of animals which had previously caused pain by using 5% formalin solution. Immunohistochemical methods were used. Since the endogenous enkephalins are considered as substances with analgesic effects that effect by binding to mu-opioid receptors in the dorsal horu of spinal cord, we expected their decreased activation in conditions of inflammatory pain. Contrary to expectations, this research has shown that, after causing inflammatory pain, there is a statistically significant increase in enkephalin concentration in the dorsaln hom of spinal cord. Although the pain was caused only on the one side of body, an increase in immunoreactivity was billateraly. These results lead us to the conclusion that, despite of the increased concentration of enkephalis, the states of hypersensitivity leads to reduced number or sensitivity of mu, and probably also delta-opioid receptors through which enkephalins effect their physiological effects. Further research is needed to gather more evidence on the above hypothesis in order to contribute to a better understanding of the role of the endogenous opiod system in inflammatory pain and ultimately result in its use in clinical practice.