Central nervous system consists of two types of cells: neurons and glial cells. Microglia, subtype of glial cells, represents supporting cells and in physiological conditions does its function as immune surveyor as well as regulator of synaptic function. Numerous studies showed the importance and role of central microglia activation in models of inflammatory and neuropathic pain. There is a lack of good animal models for the chronic musculoskeletal pain and most of the available models study acute pain of that type. Pain originating from muscle differs from cutaneous pain, by symptoms and duration, but also because of different projection from primary afferents to dorsal horn laminae which makes it special among the other types of pain. Microglial activation leads to proliferation and morphological changes, as well as changes in expression of cell surface markers, receptors and signalling pathways. Thereby, starting inflammation, or release of inflammatory mediators, contributes to development of sensitization, hyperalgesia and allodynia as main characteristics of neuropathic and inflammatory chronic pain. In this diploma thesis, activation of microglia was examined with immunohistochemical method in the samples of tissue of spinal dorsal horn for the control group and group with chronic musculoskeletal inflammatory pain. Pain was caused by intramuscular injection of 3% carragenan solution and activation of microglia was observed 21 day after the injection. Results showed that, in observed time point, there is no central microglia activation, despite development of bilateral hypersensitivity on mechanical stimuli. There are several possible explanations for this result, but the most likely is that micorglia activates in acute phase, immediately after tissue injury, contributes to the transition of acute to chronic pain, but does not participate in its maintenance. Further investigation is needed to clear the role of microglia, as well as actrocytes in initiation and maintenance of chronic musculoskeletal pain.