Expression of the FGF2 and TIMP1 Genes in the Adult Rat Brain after Administration of Interleukin-1β during Early Postnatal Ontogeny

Hypotheses relating to the developmental nature of cognitive impairments in schizophrenia and other neuropathologies propose that the development of stable cognitive deficit involves important roles for hypoxia, trauma, and infections operating during the prenatal and early postnatal periods. These pathological states are accompanied by increases in the production of proinflammatory cytokine interleukin-1β (IL-1β) in cells of the nervous and immune systems. We report here studies of the characteristics of the expression of the Fgf1 and Timp1 genes, which are involved in regulating the cerebral mechanisms of neuroplasticity, in cells of the medial prefrontal cortex and the dorsal and ventral areas of the hippocampus in adult rats given IL-1β during early postnatal ontogeny. Experiments were performed in standard conditions and on acquisition of a conditioned active avoidance reflex. Learning impairments in experimental animals were accompanied by decreased production of FGF-2 mRNA in cells of the medial prefrontal cortex and ventral hippocampus. There were no differences between groups in conditions without cognitive loading.