CSF-1 deficiency in mice results in abnormal brain development

摘要: Colony stimulating factor-1 (CSF-1) was initially identified as a growth factor for mononuclear phagocytes. This study examines the role of CSF-1 in development central nervous system (CNS). treatment neurons cultured from embryonic brain promoted survival and process outgrowth dose-dependent manner. By contrast, osteopetrotic (op/op) mouse, null mutant CSF-1, significantly less outgrowth, suggesting that there are neural abnormalities op/op animals. Nuclease protection assays were used to determine whether its receptor expressed at times appropriate regulate development. Both developing mouse brain, with unique pattern mRNA splice variant expression encoding secreted, not membrane-bound, factor. To function is altered by mutation mice examined using electrophysiologic assays. Brainstem auditory visual evoked potentials both abnormal mice. Further, intracortical recordings revealed aberrant neuronal within cortex alterations cortical circuitry balances excitation inhibition. Daily injection postnatal largely rescued phenotype, confirming absence during responsible abnormalities. The effects on cells, developmentally receptor, neurological suggest