The mechanisms of Hebbian synaptic plasticity have been widely hypothesized to play a role in the activity-dependent development of neural circuits. However, these mechanisms are inherently unstable and would lead to the runaway excitation or depression of circuits if left unchecked. In the last decade, a number of elegant studies have demonstrated that homeostatic plasticity mechanisms exist to stabilize neural networks and maintain the constancy of neuronal output in response to changes in activity levels. These include synaptic scaling, sliding threshold models of synaptic plasticity, dynamic regulation of the number and strength of synapses, and bidirectional control of intrinsic excitability. Recently, we showed that the total synaptic input onto individual neurons of the mouse superior colliculus is preserved regardless of the size of their visual receptive fields, a phenomenon we term 'response homeostasis'. Here, we argue that regulating the capacity for synaptic plasticity and controlling the number and strength of retinocollicular inputs can preserve collicular neuron output, and we present evidence that changes in intrinsic excitability are not associated with response homeostasis. We also review findings from a number of different mutant mice and discuss whether and how different cellular mechanisms may underlie response homeostasis. Combined with other studies, our work reveals an important role for homeostatic mechanisms in regulating functional connectivity during the construction of receptive fields and the refinement of topographic maps.