The time course of this drop and recovery was cell type specific, was correlated with changes in mEPSC amplitude, and was manifested across sleep-wake states. These data establish that homeostatic mechanisms within the intact CNS act to stabilize selleck kinase inhibitor neuronal firing rates in the face of sensory perturbations. Because we followed ensemble average firing rates, we do not know for certain that the average firing rates of individual neurons are restored to their predeprivation values. It is suggestive that the distribution of average firing

rates for baseline and MD6 is indistinguishable (Figure 2E), consistent with the interpretation that homeostatic regulation of firing in vivo is a cell-autonomous process that restores individual neurons back to an individual set point. However, we cannot exclude the alternative possibility that it is the

ensemble average that is regulated, while firing rates of individual neurons change over time and come to occupy a different point in the distribution. This would necessitate some kind of competitive network-level mechanism that enhances average firing of some neurons at the Idelalisib concentration expense of others to maintain the ensemble average (Hirase et al., 2001). While no such circuit-level mechanism has been identified within neocortex, there is strong evidence that neocortical neurons express cell-autonomous forms of homeostatic plasticity that could serve to regulate average firing (Desai et al., 2002, Maffei and Turrigiano, 2008 and Lambo and Turrigiano, 2013). Thus, the most likely scenario is that firing rate homeostasis

is implemented in a cell-autonomous manner and that there is a broad distribution of firing rate set points across neocortical neurons. Interestingly, heterogeneity in the homeostatic set point has been shown to improve performance in a network model of working memory (Renart et al., 2003), suggesting that this heterogeneity could be of biological significance. Acute lid suture abolishes stimulus-driven activity but has little effect on spontaneous thalamic firing rates (Linden et al., 2009), which may in part explain why there is no immediate drop in RSU firing on MD1. A MYO10 second important factor is the drop in firing of pFS cells at MD1, which may temporarily boost RSU activity by reducing inhibition from FS cells. Over time the desynchronized pre- and postsynaptic firing induced by lid suture is predicted to induce LTD (Linden et al., 2009), and the drop in RSU firing on MD2 correlates well with the induction of LTD within V1. Two days of MD during the critical period (P21–P33) induces depression of thalamocortical and intracortical excitatory synapses (Heynen et al., 2003, Khibnik et al., 2010, Maffei and Turrigiano, 2008 and Wang et al.