Deprivation-Induced Homeostatic Spine Scaling In Vivo Is Localized to Dendritic Branches that Have Undergone Recent Spine Loss

Synaptic scaling is a key homeostatic plasticity mechanism and is thought to be involved in the regulation of cortical activity levels. Here we investigated the spatial scale of homeostatic changes in spine size following sensory deprivation in a subset of inhibitory (layer 2/3 GAD65-positive) and excitatory (layer 5 Thy1-positive) neurons in mouse visual cortex. Using repeated in vivo two-photon imaging, we find that increases in spine size are tumor necrosis factor alpha (TNF-α) dependent and thus are likely associated with synaptic scaling. Rather than occurring at all spines, the observed increases in spine size are spatially localized to a subset of dendritic branches and are correlated with the degree of recent local spine loss within that branch. Using simulations, we show that such a compartmentalized form of synaptic scaling has computational benefits over cell-wide scaling for information processing within the cell. •Inhibitory and excitatory neurons exhibit TNF-α-dependent spine size increases•Spine size increases occur in a subset of dendritic branches after deprivation•Increases in spine size are correlated with local spine loss within a branch•Simulations show that branch-specific plasticity increases information processing Barnes et al. show that TNF-α-dependent spine size increases are correlated with recent spine loss within dendritic branches in both inhibitory and excitatory cortical neurons in vivo following visual deprivation. Branch-specific plasticity increases information processing relative to global plasticity.