Size-Dependent Axonal Bouton Dynamics following Visual Deprivation In Vivo

Sammons, Rosanna P.; Clopath, Claudia; Barnes, Samuel J.

doi:10.1016/j.celrep.2017.12.065

Cited by 22 publications

(16 citation statements)

References 38 publications

(64 reference statements)

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“…This diversity is manifested in the broad distri-butions of many functional and morphological properties, such as postsynaptic current amplitude, dendritic spine volume and postsynaptic density (PSD) area. Such distributions are not only broad but also rightward skewed and heavy-tailed, and are often described as log-normal (Murthy et al, 1997;Song et al, 2005;Arellano et al, 2007;Lefort et al, 2009;Minerbi et al, 2009;Loewenstein et al, 2011;Ikegaya et al, 2013;Keck et al, 2013;Statman et al, 2014;Cossell et al, 2015;Zhang et al, 2015;Hobbiss et al, 2018;Ishii et al, 2018;Masch et al, 2018;Sakamoto et al, 2018;Sammons et al, 2018;Wegner et al, 2018;Santuy et al, 2018; for review, see Barbour et al, 2007;Buzsáki and Mizuseki, 2014;Scheler, 2017). Such distributions, reflecting of a majority of weak/small synapses and a diminishing tail of increasingly stronger/larger synapses, were suggested to optimize storage capacity, neuronal firing rates and long-distance information transfer and thus impart important properties to neuronal networks (Song et al, 2005;Barbour et al, 2007;Lefort et al, 2009;Ikegaya et al, 2013;Buzsáki and Mizuseki, 2014;Scheler, 2017;Humble et al, 2019).…”

Section: Introductionmentioning

confidence: 99%

Activity Dependent and Independent Determinants of Synaptic Size Diversity

Hazan

Ziv

2020

J. Neurosci.

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The extraordinary diversity of excitatory synapse sizes is commonly attributed to activity-dependent processes that drive synaptic growth and diminution. Recent studies also point to activity-independent size fluctuations, possibly driven by innate synaptic molecule dynamics, as important generators of size diversity. To examine the contributions of activity-dependent and independent processes to excitatory synapse size diversity, we studied glutamatergic synapse size dynamics and diversification in cultured rat cortical neurons (both sexes), silenced from plating. We found that in networks with no history of activity whatsoever, synaptic size diversity was no less extensive than that observed in spontaneously active networks. Synapses in silenced networks were larger, size distributions were broader, yet these were rightward-skewed and similar in shape when scaled by mean synaptic size. Silencing reduced the magnitude of size fluctuations and weakened constraints on size distributions, yet these were sufficient to explain synaptic size diversity in silenced networks. Model-based exploration followed by experimental testing indicated that silencing-associated changes in innate molecular dynamics and fluctuation characteristics might negatively impact synaptic persistence, resulting in reduced synaptic numbers. This, in turn, would increase synaptic molecule availability, promote synaptic enlargement, and ultimately alter fluctuation characteristics. These findings suggest that activity-independent size fluctuations are sufficient to fully diversify glutamatergic synaptic sizes, with activity-dependent processes primarily setting the scale rather than the shape of size distributions. Moreover, they point to reciprocal relationships between synaptic size fluctuations, size distributions, and synaptic numbers mediated by the innate dynamics of synaptic molecules as they move in, out, and between synapses.

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Section: Introductionmentioning

confidence: 99%

Activity Dependent and Independent Determinants of Synaptic Size Diversity

Hazan

Ziv

2020

J. Neurosci.

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“…In order to study whether there were also changes in the output of GAD67‐EGFP neurons, we quantified the density of en passant boutons in EGFP expressing axons in the layer I of V1 (Figure a,b), the major projection field of these interneuronal subpopulation. Moreover, we quantified the size and fluorescence intensity (which is directly related to the size) of axonal boutons, structural readouts of cortical reorganization by experience‐dependent plasticity (Sammons, Clopath, & Barnes, ). No significant differences were found when comparing the deprived animals with their controls regarding the density of axonal boutons (Figure c; p = .657).…”

Section: Resultsmentioning

confidence: 99%

Dark exposure affects plasticity‐related molecules and interneurons throughout the visual system during adulthood

Carceller

Guirado

Nácher

2019

J of Comparative Neurology

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Several experimental manipulations, including visual deprivation, are able to induce critical period‐like plasticity in the visual cortex of adult animals. In this regard, many studies have analyzed the effects of dark exposure in adult animals, but still little is known about the role of interneurons and plasticity‐related molecules on such mechanisms. In this study, we analyzed the effects of 10 days of dark exposure on the connectivity and structure of interneurons, both in the primary visual cortex and in the rest of cerebral regions implicated in the transmission of visual stimulus. We found that this environmental manipulation induces changes in the expression of synaptic molecules throughout the visual pathway and in the structure of interneurons in the primary visual cortex. Moreover, we found altered expression in the polysialylated form of the neural cell adhesion molecule and in perineuronal nets surrounding parvalbumin expressing interneurons, suggesting that these plasticity‐related molecules may be involved in the changes produced by dark exposure. Together, our findings indicate that dark exposure produces an important alteration of inhibitory circuits and molecules related to their plasticity, not only in the visual cortex but throughout the visual pathway.

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“…This finding is consistent with those of other studies. 23 Sammons et al 8 found that LTP and long-term depression were higher in deprived versus control cortexes, indicating that MD increases plasticity in the deprived cortex. Furthermore, LTP was increased in the contralateral visual cortex by 76% after MD in cPKCγ +/+ mice but increased by only 32% in cPKCγ −/− mice.…”

Section: Discussionmentioning

confidence: 99%

“… 6 Similar studies using P17 mice have shown that MD strengthens excitatory synaptic connections of layer 4 7 and induces plasticity in layers 2 and 3 of the deprived cortex. 8 However, some studies have shown that, after MD, miniature inhibitory postsynaptic currents (IPSCs) and the density of postsynaptic GABA A receptors were increased in layer 4 of the visual cortex, 9 indicating that the plasticity of the visual cortex was decreased after MD. Thus, how visual cortex plasticity changes after MD is incompletely understood.…”

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confidence: 99%

Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCγ-Modulated GluR1 Phosphorylation in Mice

Zhang

Han

et al. 2020

Invest. Ophthalmol. Vis. Sci.

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Purpose To determine how visual cortex plasticity changes after monocular deprivation (MD) in mice and whether conventional protein kinase C gamma (cPKCγ) plays a role in visual cortex plasticity. Methods cPKCγ membrane translocation levels were quantified by using immunoblotting to explore the effects of MD on cPKCγ activation. Electrophysiology was used to record field excitatory postsynaptic potential (fEPSP) amplitude with the goal of observing changes in visual cortex plasticity after MD. Immunoblotting was also used to determine the phosphorylation levels of GluR1 at Ser831. Light transmission was analyzed using electroretinography to examine the effects of MD and cPKCγ on mouse retinal function. Results Membrane translocation levels of cPKCγ significantly increased in the contralateral visual cortex of MD mice compared to wild-type (WT) mice ( P < 0.001). In the contralateral visual cortex, long-term potentiation (LTP) and the phosphorylation levels of GluR1 at Ser 831 were increased in cPKCγ +/+ mice after MD. Interestingly, these levels could be downregulated by cPKCγ knockout compared to cPKCγ +/+ +MD mice ( P < 0.001). Compared to the right eyes of WT mice, the amplitudes of a-waves and b-waves declined in deprived right eyes of mice after MD ( P < 0.001). There were no significant differences when comparing cPKCγ +/+ and cPKCγ −/− mice with MD. Conclusions cPKCγ participates in the plasticity of the visual cortex after MD, which is characterized by increased LTP in the contralateral visual cortex, which may be a result of cPKCγ-mediated phosphorylation of GluR1 at Ser 831.

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Size-Dependent Axonal Bouton Dynamics following Visual Deprivation In Vivo

Cited by 22 publications

References 38 publications

Activity Dependent and Independent Determinants of Synaptic Size Diversity

Activity Dependent and Independent Determinants of Synaptic Size Diversity

Dark exposure affects plasticity‐related molecules and interneurons throughout the visual system during adulthood

Monocular Deprivation Affects Visual Cortex Plasticity Through cPKCγ-Modulated GluR1 Phosphorylation in Mice

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