Steroid hormones influence neuronal structure and function throughout the animal kingdom, via highly conserved receptor proteins. Insights into steroid effects on neurons and behavior have come from a range of vertebrate species including reptiles, amphibians, fish, birds, rodents and primates. In many instances, steroid hormones regulate the volume of particular regions of the nervous system by affecting both the number of constituent neurons and their size. A major determinant of neuronal number is the process of programmed cell death (PCD), which involves molecular machinery that is conserved across species. This article reviews steroid-mediated PCD and dendritic remodeling during metamorphosis of the hawkmoth, Manduca sexta. Metamorphosis is driven by a class of steroid hormones, the ecdysteroids. During the transformation from larva to pupa to adult moth, accessory planta retractor (APR) motoneurons of Manduca undergo dendritic regression and regrowth, and segment-specific PCD, in response to specific ecdysteroid cues. Experiments utilizing APRs in primary cell culture show that PCD is a direct response to ecdysteroids, regulated by the intrinsic segmental identity of individual APRs. As in other systems, activation of caspases (cysteine proteases) is involved in the execution phase of PCD. Other experiments demonstrate that the ecdysteroid-mediated regression of APRs' dendrites at pupation causes weakening of monosynaptic excitatory inputs from sensory neurons that trigger a larval withdrawal reflex. Thus, the steroid-mediated reduction in dendritic extent is linked to a specific electrophysiological and behavioral change during metamorphosis. The comparative approach, taking advantage of a variety of vertebrate and invertebrate species, holds the most promise for elucidating the full spectrum of steroid effects on neurons and behavior.