The Effects of Variable Levels of p75 Expression on Aberrant Sympathetic Axon Sprouting Into Sensory Ganglia of Mice Overexpressing Levels of NGF Production
neuroscience , p75 , Neurotrophin , sympathetic sprouting , nerve growth factor
Growth and regeneration of nervous tissue in adult mammalian organisms is limited to a few locations in the body, and to special circumstances that induce proliferation. One way that neuronal trophism can be initiated is by overexpressing the gene coding for Nerve Growth Factor (NGF) under active promoters, causing an aberrant growth of sympathetic axons into the sensory ganglia of an animal. This phenomenon has been shown in certain environments in the presence of p75 neurotrophin receptor and found to be missing in absence of the same receptor. However, previous research has not looked at situations where only one allele of the p75 Neurotrophin Receptor (p75NTR) is present. To fill this gap in the literature, a rodent model with elevated levels of NGF, and a single functioning allele of p75NTR was investigated and quantitatively assessed against its genetically alternate littermates to determine the impact on sympathosensory sprouting in animals having one mutated p75NTR allele. It was discovered that while the mutation of the p75NTR allele had minimal impact on the morphology of sympathosensory sprouting into the brains of these animals, it induced not only greater sympathetic sprouting into sensory ganglia than its wildtype and knockout counterparts, but also augmented the density of the peculiar perineuronal plexuses found forming around a subset of sensory neurons within the dorsal root ganglia and the trigeminal ganglia. This study suggests that satellite glial cells are a key component of sympathosensory sprouting, and that the gain-of-function mutation within these heterozygous animals could be used as a model for further research into sympathetically maintained pain.