TrkA-expressing trigeminal sensory neurons display both neurochemical and structural plasticity despite a loss of p75(NTR) function: responses to normal and elevated levels of nerve growth factor

In neural crest-derived sensory ganglia, approximately half of the neuronal population expresses the transmembrane trkA receptor that is required for neuronal binding of target-derived nerve growth factor (NGF). These same ne urons also express the p75 neurotrophin receptor (NTR) that increases the a ffinity of trkA for NGF. Depleting p75(NTR) expression reduces both the sur vival of trkA-positive sensory neurons and their afferent innervation of pe ripheral targets. in this investigation, we assessed the neurochemical and structural plasticity of trigeminal sensory neurons in p75(NTR)-deficient m ice in response to either normal or elevated levels of NGF during postnatal development and into adulthood. Although p75(NTR)-deficient mice have 30% fewer trigeminal neurons, levels of trkA mRNA expression are modestly eleva ted in these mutant mice as compared to control mice. The density of centra l afferent axons and local levels of NGF are, however, comparable between m utant and control animals. Thus, despite the survival of fewer trigeminal n eurons, neither ganglionic levels of trkA mRNA expression nor the density o f central afferent projections are depleted in p75(NTR)-deficient mice. In response to elevated levels of NGF protein, transgenic mice with and withou t p75(NTR) expression display both increased levels of trkA mRNA expression and a greater density of trigeminal central afferent axons as compared to control mice. These data further reveal that an absence of p75(NTR) functio n in trigeminal sensory neurons does not diminish their capacity for NGF-de pendent plasticity, namely trkA mRNA expression and collateral growth of ce ntral afferent axons.