Children's and adults' cognitive dysfunctions are frequently caused by various types of pathology such as birth injuries, hypoxias, and infections suffered in prenatal and early postnatal periods of ontogenesis. These abnormal conditions trigger high production of proinflammatory cytokines by the cells of nervous and immune systems. The role of interleukin-1 beta (IL-1beta), one of such proteins, in the formation of cognitive deficit in early ontogenesis is not sufficiently studied. In present research it was revealed that administration of IL-1beta during the third week of postnatal ontogenesis impaired the learning of adult rats in Morris Water Maze. The differences between rats of control and experimental groups were observed during the training of searching for hidden platform and during the alteration of formed reflex (when the platform was in a different place). Meanwhile the spatial extinction has not been disrupted. The nature of experimental rats' learning abnormalities allows us to assume that the mechanisms of long-term but not short-term spatial memory are damaged in this experimental situation.