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• W1488963453 abstract "Adjustments in neural activity can drive cortical plasticity, but the underlying circuit components remain unclear. In this issue of Neuron, Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar show that visual deprivation-induced homeostatic plasticity invokes specific changes among select categories of V1 neurons. Adjustments in neural activity can drive cortical plasticity, but the underlying circuit components remain unclear. In this issue of Neuron, Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar show that visual deprivation-induced homeostatic plasticity invokes specific changes among select categories of V1 neurons. The brain has evolved extensive mechanisms to maintain stable activity levels in the face of fluctuating synaptic drive. Indeed, when these mechanisms fail, devastating consequences can occur such as runaway excitation and epilepsy. At the same time, there are a number of instances in which neural circuits need to greatly increase their levels of activation, such as during sensory plasticity. How does the brain reconcile these seemingly contradictory needs? One way is through homeostatic plasticity or the ability to fine tune the excitability of specific neuronal networks (Turrigiano, 2012Turrigiano G. Cold Spring Harb. Perspect. Biol. 2012; 4: a005736Crossref Scopus (643) Google Scholar). In this issue of Neuron, Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar addressed whether homeostatic recovery of cortical activity in response to visual deprivation reflects the involvement of specific subsets of neurons and how those cells contribute to the plasticity of the larger circuits in which they are embedded. Classic paradigms for manipulating sensory drive and cortical plasticity, such as eye-lid suture, dark rearing, or retinal lesions, have been shown to trigger homeostatic regulation of firing rate in the developing (Desai et al., 2002Desai N.S. Cudmore R.H. Nelson S.B. Turrigiano G.G. Nat. Neurosci. 2002; 5: 783-789PubMed Google Scholar, Hengen et al., 2013Hengen K.B. Lambo M.E. Van Hooser S.D. Katz D.B. Turrigiano G.G. Neuron. 2013; 80: 335-342Abstract Full Text Full Text PDF PubMed Scopus (201) Google Scholar) and in the mature (Keck et al., 2013Keck T. Keller G.B. Jacobsen R.I. Eysel U.T. Bonhoeffer T. Hübener M. Neuron. 2013; 80: 327-334Abstract Full Text Full Text PDF PubMed Scopus (191) Google Scholar) neocortex. While there is general agreement that both excitatory and inhibitory mechanisms are at play, until recently it was challenging to tackle the cell-type-specific dynamics of homeostatic plasticity in the intact brain—in large part because such events occur over a period of several days or longer. However, due to recent advances in optical and other neuronal recording techniques, it is now possible to monitor the activity of large populations of identified cells in intact, awake behaving animals and to correlate the observed changes with molecular, connectivity, or structural analysis post hoc (e.g., Bock et al., 2011Bock D.D. Lee W.C. Kerlin A.M. Andermann M.L. Hood G. Wetzel A.W. Yurgenson S. Soucy E.R. Kim H.S. Reid R.C. Nature. 2011; 471: 177-182Crossref PubMed Scopus (596) Google Scholar, Ko et al., 2013Ko H. Cossell L. Baragli C. Antolik J. Clopath C. Hofer S.B. Mrsic-Flogel T.D. Nature. 2013; 496: 96-100Crossref PubMed Scopus (258) Google Scholar). In this issue of Neuron, Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar used a powerful combination of in vivo and ex vivo approaches to explore the cell-type-specific changes that underlie sensory-driven homeostatic plasticity in the visual system. The authors imaged the activity of mouse primary visual cortex (V1) neurons expressing the genetically encoded calcium indicator GCaMP5 in awake behaving mice while the mice viewed patterned stimuli. Using this approach they were able to chronically measure the activity of the same individual neurons located in layer 2/3 both before and after monocular enucleation. They noted that prior to any visual deprivation, V1 cells displayed heterogeneous profiles of calcium transient kinetics—some were very slow and some were fast—and they hypothesized that those differences represent excitatory versus inhibitory neurons, respectively. Indeed, by staining V1 for the inhibitory transmitter GABA after the conclusion of the imaging experiments, they were able to confirm that it was the inhibitory V1 neurons that had faster calcium kinetics. This gave them a nice handle on the ability to monitor these two general categories of cell types in vivo and thereby address the relative roles and timescales over which inhibitory and excitatory neurons contribute to homeostatic plasticity, as well as how those two forces interact. Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar found that soon after monocular enucleation, the overall activity of cells in the region of V1 corresponding to the deprived-eye pathway initially plummeted but then recovered after 48–72 hr (summarized in Figures 1A–1C). By analyzing the activity profiles of individual neurons, however, they discovered that only a subset of layer 2/3 cells actually undergoes homeostatic recovery (Figure 1C). Many inhibitory neurons in V1 became and stayed inactive after deprivation, whereas others reduced and then partially recovered their output but never back to their pre-deprivation levels. Thus, unlike the scenario in developing V1 (Hengen et al., 2013Hengen K.B. Lambo M.E. Van Hooser S.D. Katz D.B. Turrigiano G.G. Neuron. 2013; 80: 335-342Abstract Full Text Full Text PDF PubMed Scopus (201) Google Scholar), inhibitory neurons in adult V1 do not undergo homeostatic recovery. These findings indicate that sensory deprivation in adulthood results in lower overall levels of inhibition. Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar confirmed this by performing whole-cell patch-clamp recordings of the inputs onto V1 excitatory neurons in acute slices. They found a reduction in the frequency of miniature inhibitory postsynaptic currents indicating that, indeed, there are fewer inhibitory synapses following monocular enucleation as compared to pre-deprivation. Not surprisingly, Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar also observed that visual deprivation shifted the excitatory/inhibitory (E/I) balance toward excitation. In several deprivation-induced plasticity paradigms, reduced synaptic inhibition has been shown to precede excitatory changes (Chen et al., 2011Chen J.L. Lin W.C. Cha J.W. So P.T. Kubota Y. Nedivi E. Nat. Neurosci. 2011; 14: 587-594Crossref PubMed Scopus (157) Google Scholar, Keck et al., 2011Keck T. Scheuss V. Jacobsen R.I. Wierenga C.J. Eysel U.T. Bonhoeffer T. Hübener M. Neuron. 2011; 71: 869-882Abstract Full Text Full Text PDF PubMed Scopus (163) Google Scholar, van Versendaal et al., 2012van Versendaal D. Rajendran R. Saiepour M.H. Klooster J. Smit-Rigter L. Sommeijer J.P. De Zeeuw C.I. Hofer S.B. Heimel J.A. Levelt C.N. Neuron. 2012; 74: 374-383Abstract Full Text Full Text PDF PubMed Scopus (155) Google Scholar), thus Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar next explored the changes that excitatory V1 neurons underwent. They observed that ∼50% of the excitatory neurons they imaged became inactive and stayed inactive, long after deprivation—i.e., they never recovered (Figures 1A–1C). However, other excitatory neurons recovered within ∼72 hr after eye removal (Figure 1C). Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar referred to these neurons as “recovering cells.” To separately examine the homeostatic mechanisms in recovering cells versus those that became and stayed inactive, they combined intracellular dye-filling of electrophysiologically recorded V1 neurons with immunolabeling for the activity marker c-Fos. They found that the presence of c-Fos expression in a neuron closely reflected the level of activity that cell displayed in vivo and thus was a good readout of highly active versus less active cells. Some V1 neurons were highly active after deprivation and expressed c-Fos, whereas most of the inactive V1 neurons did not express c-Fos. Interestingly, synaptic inhibition was reduced onto both the c-Fos-expressing and the c-Fos-negative groups of neurons. This suggests that diminished synaptic inhibition alone cannot explain the fact that some excitatory cells recover and others do not. This is a particularly novel finding given the large body of work pointing to inhibition as a major driving force for plasticity. Thus, Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar discovered that homeostatic recovery of activity in response to visual deprivation does not occur equally between excitatory versus inhibitory neurons, nor does it impact all excitatory neurons in the same way. Why did some excitatory cells recover and others did not? In recent years, several groups have unveiled “subnetworks” of highly interconnected cortical neurons that are activated by common stimuli and/or input pathways (Ko et al., 2011Ko H. Hofer S.B. Pichler B. Buchanan K.A. Sjöström P.J. Mrsic-Flogel T.D. Nature. 2011; 473: 87-91Crossref PubMed Scopus (519) Google Scholar, Miller et al., 2014Miller J.E. Ayzenshtat I. Carrillo-Reid L. Yuste R. Proc. Natl. Acad. Sci. USA. 2014; 111: E4053-E4061Crossref PubMed Scopus (162) Google Scholar, Yoshimura et al., 2005Yoshimura Y. Dantzker J.L. Callaway E.M. Nature. 2005; 433: 868-873Crossref PubMed Scopus (451) Google Scholar). Are cortical subnetworks also activated during adult homeostatic plasticity? Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar measured the correlation of GCaMP5 signals in V1 cells prior to enucleation and found that certain groups of these neurons tended to display synchronous activity. Remarkably, the subsets of excitatory neurons that they observed undergoing homeostatic recovery tended to be the same ones that participated in highly correlated networks at the outset of the experiment. In a similar and equally interesting vein, the excitatory neurons that failed to recover after deprivation tended to exhibit activity that, at the outset of the experiment (pre-deprivation), was correlated to other non-recovering cells (Figures 1A and 1C). These results were surprising given that, normally, sensory-driven cortical ensembles are highly dynamic—recruiting new cells and synaptic interactions depending on stimulus conditions (Miller et al., 2014Miller J.E. Ayzenshtat I. Carrillo-Reid L. Yuste R. Proc. Natl. Acad. Sci. USA. 2014; 111: E4053-E4061Crossref PubMed Scopus (162) Google Scholar). The findings of Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar argue that sensory deprivation-induced plasticity invokes relatively fixed groups of strongly correlated cells and interactions among them. Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar also examined the correlations that existed between the excitatory and inhibitory groups of neurons and found that groups that were highly correlated prior to deprivation tended to remain so even after plasticity, albeit with the reduced levels of inhibition that exist compared to non-deprived conditions (Figure 1C). As a consequence of this, the subnetworks of excitatory neurons that recovered activity tended to be correlated with inhibitory neurons that managed to maintain some level of activity after deprivation (Figure 1C). Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar also explored for evidence that other mechanisms such as synaptic scaling are involved in driving homeostatic recovery. They found no changes in miniature excitatory postsynaptic potential frequency or amplitude, spine size or density, or intrinsic excitability of V1 cells. That, coupled with the changes they did observe in select groups of highly correlated neurons (Figures 1A–1C), led them to the conclusion that local network activity plays a key role in the homeostatic recovery to sensory deprivation in adult V1. A critical next step for the field is to understand whether this network activity is not just reflective of, but necessary for, homeostatic plasticity and if so what feature(s) of the subnetworks are crucial. New techniques that allow for the selective activation and silencing of neurons based on their activity profiles (Guenthner et al., 2013Guenthner C.J. Miyamichi K. Yang H.H. Heller H.C. Luo L. Neuron. 2013; 78: 773-784Abstract Full Text Full Text PDF PubMed Scopus (324) Google Scholar, Packer et al., 2015Packer A.M. Russell L.E. Dalgleish H.W. Häusser M. Nat. Methods. 2015; 12: 140-146Crossref PubMed Scopus (344) Google Scholar) may be useful in this context by allowing replay or inhibition of the relevant members of highly active cortical subnetworks. Barnes et al., 2015Barnes S.J. Sammons R.P. Jacobsen R.I. Mackie J. Keller G.B. Keck T. Neuron. 2015; 86 (this issue): 1290-1303Abstract Full Text Full Text PDF PubMed Scopus (59) Google Scholar suggest that the interconnections between cells in a subnetwork or the common inputs they share might influence whether they can recover after deprivation. Therefore, it will also be important to identify differences among the sources of synaptic input to the recovering versus non-recovering cells. Furthermore, understanding how local subnetwork activity influences homeostatic synaptic plasticity may prove important for developing new therapeutic approaches to help re-establish broken neural circuits and treat neurological conditions and disorders. Subnetwork-Specific Homeostatic Plasticity in Mouse Visual Cortex In VivoBarnes et al.NeuronJune 03, 2015In BriefBarnes et al. examine homeostatic recovery of activity of individual excitatory and inhibitory neurons in the adult cortex following enucleation. A fraction of excitatory neurons recover activity, in a subnetwork specific manner, but inhibitory cells do not recover activity over 72 hr. Full-Text PDF Open Access" @default.
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• W1488963453 title "Cortical Cliques: A Few Plastic Neurons Get All the Action" @default.
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