We examined the age-dependent morphological changes of lumbar spinal motoneurons (MNs) in neonatal Swiss-Webster mice during the first 2 weeks of postnatal life. Neurons labeled by intracellular injection of biocytin in hemisected lumbosacral spinal cords in vitro were reconstructed from serial sections. Digitized data were compared for young (P3; postnatal days 2-4; n ϭ 9) and older animals (P11; postnatal days 10 -13; n ϭ 8). As expected, measures of dendritic size (e.g., stem branch diameter, total surface area, maximum distance to tips, and lateral tree spread) were all significantly greater for P11 than for P3 mice. In contrast, the number of dendrites per MN and parameters related to tree topology (e.g., terminations per tree and maximum branch order), although slightly greater for P11 animals, were not significantly different between the two ages. Dendrite growth appeared to be proportional throughout the tree because the ratios between average terminal and internal branch lengths were similar for the two groups. Furthermore, this elongation was proportional to enlargement of overall spinal cord dimensions. A variety of other morphometric measures showed no significant difference between age groups. The relative constancy of MN dendritic topology up to P13 was surprising, given the striking maturation in motor function during this time period. J. Comp. Neurol. 483:304 -317, 2005 Dendrites are essential elements in understanding neural network connectivity and input/output properties of individual neurons in the central nervous system (see Stuart et al., 2001). Much of our current understanding of the linkage between dendritic morphology and the biophysics of electrotonic current flows within neuronal dendrites is based on early studies of spinal motoneurons (MNs) (Rall, 1959(Rall, , 1960(Rall, , 1977Burke and ten Bruggencate, 1971;Iansek and Redman, 1973;Jack et al., 1975). Aside from historical importance, the influence of MN dendrite morphology on the input/output relations of these cells is clearly relevant to understanding the control of motor unit recruitment. In addition, their involvement in amyotrophic lateral sclerosis (ALS) and other motor neuron diseases has generated considerable interest in the structural and functional development of mammalian MNs in fetal (Allan and Greer, 1997) and early postnatal life (Cameron and He, 1989;Curfs et al., 1993; Nuñ ez-Abades et al., 1993Nuñ ez-Abades and Cameron, 1995;Ramirez and Ulfhake, 1991;Walton and Navarrete, 1991; reviewed in Cameron and Nuñ ez-Abades, 2000).Because of the availability of spontaneous and genetically engineered neurological mutants, the mouse has become a key model species for studies of the influence of specific molecular pathways in the development and maintenance of neuronal dendrites (e.g