Dendrite development is controlled by the interplay of intrinsic and extrinsic signals affecting initiation, growth, and maintenance of complex dendrites. Bone morphogenetic proteins (BMPs) stimulate dendrite growth in cultures of sympathetic, cortical, and hippocampal neurons but it was unclear whether BMPs control dendrite morphologyin vivo. Using a conditional knock-out strategy to eliminateBmpr1aandSmad4in immature noradrenergic sympathetic neurons we now show that dendrite length, complexity, and neuron cell body size are reduced in adult mice deficient ofBmpr1a. The combined deletion ofBmpr1aandBmpr1bcauses no further decrease in dendritic features. Sympathetic neurons devoid ofBmpr1a/1bdisplay normal Smad1/5/8 phosphorylation, which suggests that Smad-independent signaling paths are involved in dendritic growth control downstream of BMPR1A/B. Indeed, in theSmad4conditional knock-out dendrite and cell body size are not affected and dendrite complexity and number are increased. Together, these results demonstrate anin vivofunction for BMPs in the generation of mature sympathetic neuron dendrites. BMPR1 signaling controls dendrite complexity postnatally during the major dendritic growth period of sympathetic neurons.