Homeostatic Regulation of Motoneuron Properties in Development

Homeostatic plasticity represents a set of compensatory mechanisms that are engaged following a perturbation to some feature of neuronal or network function. Homeostatic mechanisms are most robustly expressed during development, a period that is replete with various perturbations such as increased cell size and the addition/removal of synaptic connections. In this review we look at numerous studies that have advanced our understanding of homeostatic plasticity by taking advantage of the accessibility of developing motoneurons. We discuss the homeostatic regulation of embryonic movements in the living chick embryo and describe the spinal compensatory mechanisms that act to recover these movements (homeostatic intrinsic plasticity) or stabilize synaptic strength (synaptic scaling). We describe the expression and triggering mechanisms of these forms of homeostatic plasticity and thereby gain an understanding of their roles in the motor system. We then illustrate how these findings can be extended to studies of developing motoneurons in other systems including the rodents, zebrafish, and fly. Furthermore, studies in developing drosophila have been critical in identifying some of the molecular signaling cascades and expression mechanisms that underlie homeostatic intrinsic membrane excitability. This powerful model organism has also been used to study a presynaptic form of homeostatic plasticity where increases or decreases in synaptic transmission are associated with compensatory changes in probability of release at the neuromuscular junction. Further, we describe studies that demonstrate homeostatic adjustments of ion channel expression following perturbations to other kinds of ion channels. Finally, we discuss work in xenopus that shows a homeostatic regulation of neurotransmitter phenotype in developing motoneurons following activity perturbations. Together, this work illustrates the importance of developing motoneurons in elucidating the mechanisms and roles of homeostatic plasticity.