Neonatal Proinflammatory Stress and the Maturation of Intercellular Communication in the Hippocampus
- PDF / 405,703 Bytes
- 13 Pages / 594 x 792 pts Page_size
- 55 Downloads / 154 Views
Neonatal Proinflammatory Stress and the Maturation of Intercellular Communication in the Hippocampus I. V. Kudryashova, M. Yu. Stepanichev, and N. V. Gulyaeva
UDC 612.822.3
Translated from Zhurnal Vysshei Nervnoi Deyatel’nosti imeni I. P. Pavlova, Vol. 69, No. 6, pp. 680–699, November–December, 2019. Original article submitted March 6, 2019. Revised version received May 15, 2019. Accepted June 3, 2019. 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. Keywords: neonatal proinflammatory stress, hippocampus, long-term plasticity, cytokines, brain-derived neurotrophic factor, glucocorticoids.
Introduction. Infectious diseases at prenatal and neonatal age create an adverse background for the development of the brain, increasing the risk of developing cerebral pathologies [Blume et al., 2011; Capuron and Miller, 2011; Krishnadas and Cavanagh, 2012; Maes et al., 2012]. For example, children born very premature due to the development of inflammatory processes such as necrotizing enterocolitis or meningitis display severe impairments to mental and physical development [van Vliet et al., 2013]. One of the risk factors is neuroinflammation associated with activation of the microglia [Krishnadas and Cavanagh, 2012; Kettenmann et al., 2013]; this activation can be maintained for long periods of time [Williamson et al., 2011; Sominsky et al., 2012; Wang et al., 2013]. The role of the microglia in the developing brain is linked with optimization of the forming neural structures due to elimination of nonfunctional or low-activity synapses and “excess” neurons [Bilimoria and Stevens, 2015; Wu et al., 2015; Mosser et al., 2017;
Tay et al., 2017]. Impairment to the normal functioning of the microglia may be one of the causes of the development of chronic brain diseases, especially autistic spectrum disorders and schizophrenia [Stephan et al., 2012; Eyo and Wu, 2013; Mosser et al., 2017; Neniskyte and Gross, 2017]. Structural-functional maturation of the higher parts of the brain occurs postnatally over a quite long period of time [Dumas, 2005], in particular, the process of synaptogenesis occurs most intensely in the hippocampu
Data Loading...
