Changes in input lead to changes of synaptic circuits in the brain via a combination of synapse specific Hebbian plasticity and cell-wide homeostatic plasticity. While Hebbian plasticity has been well studied, there are still a number of outstanding fundamental questions related to homeostatic plasticity. We have previously developed a paradigm that allows us to monitor changes to multiple homeostatic mechanisms in the intact mouse visual cortex following sensory deprivation. We will use this paradigm together with chronic two-photon imaging of synaptic structures and function, via genetically encoded calcium indicators in awake behaving animals. These techniques allow us to measure the structure and function from the same synapses and cells over a period of weeks to months, both before and after sensory deprivation. In the work proposed here, we will investigate two basic principles of homeostatic plasticity: 1) the spatial scale at which homeostatic mechanisms occur – is it at the level of individual dendrites or are all changes implemented cell-wide? and 2) the relationship between homeostatic plasticity and the degree of changing activity levels in cells and networks of cells – is the degree of resulting homeostatic plasticity dependent on the level of deprivation? If so, can changes in dendritic activity, cellular activity or network activity drive these changes? We will investigate these questions for both excitatory and inhibitory neurons in the intact mouse visual cortex for two forms of homeostatic plasticity – synaptic scaling and the balance between excitation and inhibition.