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

Barnes, Samuel J.; Franzoni, Eleonora; Jacobsen, R. Irene; Erdélyi, Ferenc; Szabó, Gábor; Clopath, Claudia; Keller, Georg B.; Keck, Tara

doi:10.1016/j.neuron.2017.09.052

Cited by 109 publications

(120 citation statements)

References 74 publications

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“…Homeostatic synaptic scaling was first demonstrated in neurons cultured from rat visual cortex (Turrigiano et al, 1998). It has since been demonstrated in vivo in the visual cortex (Barnes et al, 2017;Desai et al, 2002;Hengen et al, 2013;Keck et al, 2013;Wallace and Bear, 2004) and during sleep (Diering et al, 2017). A recent study, however, demonstrated that visual deprivation by eyelid suture elevates spontaneous activity and lowers the threshold for LTP, a form of homeostatic plasticity distinct from synaptic scaling called "metaplasticity," or the sliding threshold model (Bridi et al, 2018).…”

Section: Homeostatic Plasticity In Vitro Versus In Vivomentioning

confidence: 99%

Homeostatic Plasticity Requires Remodeling of the Homer-Shank Interactome

We¹,

Speed²,

Jd³

et al. 2020

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Neurons maintain constant levels of excitability using homeostatic scaling, which adjusts relative synaptic strength in response to large changes in overall activity. While previous studies have catalogued the transcriptomic and proteomic changes associated with scaling, the resulting alterations in synaptic protein interaction networks (PINs) are less well understood. Here, we monitor a glutamatergic synapse PIN composed of 380 binary interactions among 21 protein members to identify protein complexes altered by synaptic scaling. In cultured cortical neurons, we observe widespread bidirectional PIN alterations with up-versus downscaling. In the barrel cortex, the PIN response to 48 hours of sensory deprivation exhibits characteristics of both upscaling and downscaling, consistent with emerging models of excitatory/inhibitory balance in cortical plasticity. Mice lacking Homer1 or Shank3B do not undergo normal PIN rearrangements, suggesting that these Autism Spectrum Disorder (ASD)-linked proteins serve as structural hubs for synaptic homeostasis. Our approach demonstrates how previously identified RNA and protein-level changes induced during homeostatic scaling translate into functional PIN alterations.

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Section: Homeostatic Plasticity In Vitro Versus In Vivomentioning

confidence: 99%

Homeostatic Plasticity Requires Remodeling of the Homer-Shank Interactome

We¹,

Speed²,

Jd³

et al. 2020

Preprint

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“…This fast, the postsynaptic neuron at any time, which leads to a competition for these building 118 blocks between synapses of the same type [44]. Although there exists evidence for SN in 119 glutamatergic and GABAergic synapses [27,28,43] as well as slow scaling [9,45] within 120 dendritic branches [46], we make the assumption that the SN in these synapses is fast, 121 and that the homeostatic change depends on the weight in a multiplicative fashion [44]. 122 The SN works as follows: all excitatory (inhibitory) weights onto a neuron are regularly 123 updated as 124 w e,j → w e,j 1 + η SN T e,e Ke m=1 w e,m…”

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confidence: 99%

Neural oligarchy: how synaptic plasticity breeds neurons with extreme influence

Kleberg

Triesch

2018

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Synapses between cortical neurons are subject to constant modifications through synaptic plasticity mechanisms, which are believed to underlie learning and memory formation. The strengths of excitatory and inhibitory synapses in the cortex follow a right-skewed long-tailed distribution. Similarly, the firing rates of excitatory and inhibitory neurons also follow a right-skewed long-tailed distribution. How these distributions come about and how they maintain their shape over time is currently not well understood. Here we propose a spiking neural network model that explains the origin of these distributions as a consequence of the interaction of spike-timing dependent plasticity (STDP) of excitatory and inhibitory synapses and a multiplicative form of synaptic normalisation. Specifically, we show that the combination of additive STDP and multiplicative normalisation leads to lognormal-like distributions of excitatory and inhibitory synaptic efficacies as observed experimentally. The shape of these distributions remains stable even if spontaneous fluctuations of synaptic efficacies are added. In the same network, lognormal-like distributions of the firing rates of excitatory and inhibitory neurons result from small variability in the spiking thresholds of individual neurons. Interestingly, we find that variation in firing rates is strongly coupled to variation in synaptic efficacies: neurons with the highest firing rates develop very strong connections onto other neurons. Finally, we define an impact measure for individual neurons and demonstrate the existence of a small group of neurons with an exceptionally strong impact on the network, that arise as a result of synaptic plasticity. In summary, synaptic plasticity and small variability in neuronal parameters underlie a neural oligarchy in recurrent neural networks. Author summaryOur brain's neural networks are composed of billions of neurons that exchange signals via trillions of synapses. Are these neurons created equal, or do they contribute in similar ways to the network dynamics? Or do some neurons wield much more power than others? Recent experiments have shown that some neurons are much more active than the average neuron and that some synaptic connections are much stronger than the average synaptic connection. However, it is still unclear how these properties come about in the brain. Here we present a neural network model that explains these findings as a result of the interaction of synaptic plasticity mechanisms that modify synapses' efficacies. The model reproduces recent findings on the statistics of neuronal firing rates PLOS

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“…The regulating process involves an enhanced accumulation of AMPAR in the postsynaptic membrane, which can be mediated by the pro-inflammatory cytokine tumour-necrosis factor-α (TNF-α) produced by glia (Stellwagen and Malenka, 2006), the immediate-early gene Arc (Shepherd et al, 2006), β3 integrins (Cingolani et al, 2008) and other molecules. Crucially, the scaling is bidirectional, global and operates in a multiplicative manner (Turrigiano et al, 1998), although there is some evidence for dendritic-branch specific scaling in some neocortical cell types (Barnes et al, 2017). During recovery, multiplicative scaling potentiates synaptic weights within assemblies more than across assemblies in our model, preserving the relative strength of synaptic inputs and enabling the recovery of correlation structure.…”

Section: Discussionmentioning

confidence: 84%

Homeostatic mechanisms regulate distinct aspects of cortical circuit dynamics

Hengen

Turrigiano

et al. 2019

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Homeostasis is indispensable to counteract the destabilizing effects of Hebbian plasticity. Although it is commonly assumed that homeostasis modulates synaptic strength, membrane excitability and firing rates, its role at the neural circuit and network level is unknown. Here, we identify changes in higher-order network properties of freely behaving rodents during prolonged visual deprivation.Strikingly, our data reveal that pairwise functional correlations and their structure are subject to homeostatic regulation. Using a computational model, we demonstrate that the interplay of different plasticity and homeostatic mechanisms can capture the initial drop and delayed recovery of firing rates and correlations observed experimentally. Moreover, our model indicates that synaptic scaling is crucial for the recovery of correlations and network structure, while intrinsic plasticity is essential for the rebound of firing rates, suggesting that synaptic scaling and intrinsic plasticity can serve distinct functions in homeostatically regulating network dynamics.

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

Cited by 109 publications

References 74 publications

Homeostatic Plasticity Requires Remodeling of the Homer-Shank Interactome

Homeostatic Plasticity Requires Remodeling of the Homer-Shank Interactome

Neural oligarchy: how synaptic plasticity breeds neurons with extreme influence

Homeostatic mechanisms regulate distinct aspects of cortical circuit dynamics

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