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© 2016 Wiley Periodicals, Inc. Dendritic morphology is a critical determinant of neuronal connectivity, and in postganglionic sympathetic neurons, tonic activity correlates directly with the size of the dendritic arbor. Thus, identifying signaling mechanisms that regulate dendritic arborization of sympathetic neurons is important to understanding how functional neural circuitry is established and maintained in the sympathetic nervous system. Bone morphogenetic proteins (BMPs) promote dendritic growth in sympathetic neurons; however, downstream signaling events that link BMP receptor activation to dendritic growth are poorly characterized. We previously reported that BMP7 upregulates p75NTRmRNA in cultured sympathetic neurons. This receptor is implicated in controlling dendritic growth in central neurons but whether p75NTRregulates dendritic growth in peripheral neurons is not known. Here, we demonstrate that BMP7 increases p75NTRprotein in cultured sympathetic neurons, and this effect is blocked by pharmacologic inhibition of signaling via BMP type I receptor. BMP7 does not trigger dendritic growth in sympathetic neurons dissociated from superior cervical ganglia (SCG) of p75NTRnullizygous mice, and overexpression of p75NTRin p75NTR−/− neurons is sufficient to cause dendritic growth even in the absence of BMP7. Morphometric analyses of SCG from wild-type versus p75NTRnullizygous mice at 3, 6, and 12 to 16 weeks of age indicated that genetic deletion of p75NTRdoes not prevent dendritic growth but does stunt dendritic maturation in sympathetic neurons. These data support the hypotheses that p75NTRis involved in downstream signaling events that mediate BMP7-induced dendritic growth in sympathetic neurons, and suggest that p75NTRsignaling positively modulates dendritic complexity in sympathetic neurons in vivo. © 2016 Wiley Periodicals, Inc. Develop Neurobiol 76: 1003–1013, 2016.