Neonatal Proinflammatory Stress and the Maturation of Intercellular Communication in the Hippocampus

Abstract

Neuroinflammatory processes, particularly those induced by infectious agents, are associated with activation of the microglia and subsequent increases in the secretion of proinflammatory cytokines. Proinflammatory stimuli acting in early postnatal ontogeny are stress factors and, along with neuroinflammation, trigger the mechanisms of the stress response. If the proinflammatory signal is sufficiently powerful, the response to it can lead to modification of the body’s stress resistance and an increase in the risk of developing psychopathology accompanied by cognitive impairments at later stages of ontogeny, including in adults. This review considers several mechanisms linked in particular with the functions of the transmitter systems and the neurotrophin, cytokine, and glucocorticoid systems, which determine maturation of intercellular communications in the hippocampus on the background of neuroinflammation and the sequelae of impairments to this process.