Inflammatory pain occurs as a result of inflammation or tissue injury which causes the secretion of various inflammatory mediators that activate nociceptors. Peripheral changes caused by inflamation result in sensitization of spinal cord neurons. Those processes, known as peripheral and central sensitization, contribute to the transition from acute to chronic pain. Electrical impulses generated by activated nociceptors on periphery are transmitted to the dorsal horn of the spinal cord,where are placed astrocytes. They are a star-shaped glia cells activated in experimental models of chronic pain and they release mediators that make contribution to the process of central sensitization. This thesis is based on measurement of astrocyte activation, using an immunohistochemical method, in tissue samples of dorsal horn of the spinal cord of animals which had previously caused chronic muscle pain by using 3% carrageenan solution. Using an immunohistochemical analysis we revealed that there is no statistically significant increase in expression of astrocytes marker (GFAP) in the dorsal horn of the spinal cord 21 day after the initial muscle injury. These results lead us to the conclusion that, unlike the chronic neuropathic pain, astrocytes do not have an important role in appearance and maintenance of chronic muscle pain. Further researches about the involvement of astrocytes in processes of development of chronic pain are needed. They should consider activation of astrocytes in different times after initial injury of deep tissues and their interaction with microglia and neurons. The results of those researches could direct development od new analgetic drugs for chronic pain on modulation of function of glia cells in central nervous system.