sincalide and Neonatal-Sepsis

Axon development plays a pivotal role in the formation of synapse, nodes of Ranvier, and myelin sheath. Interleukin-1β (IL-1β) produced by microglia may cause myelination disturbances through suppression of oligodendrocyte progenitor cell maturation in the septic neonatal rats. Here, we explored if a microglia-derived IL-1β would disturb axon development in the corpus callosum (CC) following lipopolysaccharide (LPS) administration, and if so, whether it is associated with disorder of synapse formation in the cerebral cortex and node of Ranvier.. Sprague-Dawley rats (1-day old) in the septic model group were intraperitoneally administrated with lipopolysaccharide (1 mg/kg) and then sacrificed for detection of IL-1β, interleukin-1 receptor (IL-1R. In 1-day old septic rats, IL-1β expression was increased in microglia coupled with upregulated expression of IL-1R. The present results suggest that microglia-derived IL-1β might suppress axon development through activation of p38-MAPK signaling pathway that would contribute to formation disorder of cortical synapses and node of Ranvier following LPS exposure.

Topics: Age Factors; Animals; Animals, Newborn; Cells, Cultured; Cerebral Cortex; Disease Models, Animal; Gene Expression Regulation; Interleukin-1beta; Lipopolysaccharides; Microglia; Neonatal Sepsis; Nerve Tissue Proteins; Neurons; p38 Mitogen-Activated Protein Kinases; Rats; Rats, Sprague-Dawley; Signal Transduction; Sincalide; Synapses; Synaptophysin