Spontaneous activations follow a common developmental course across primary sensory areas in mouse neocortex

Frye, Charles G.; MacLean, Jason N.

doi:10.1152/jn.00172.2016

Cited by 14 publications

(13 citation statements)

References 42 publications

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“…Third, our model predicts that as a result of receptive field refinement during development, network events sparsify as global, cortically generated events are attenuated and become more localized. Interestingly, the properties of spontaneous activity measured experimentally in different sensory cortices [33,57,92,93,94,34] and in the olfactory bulb [87] change following a very similar timeline during development as predicted in our model. However, in many of these studies activity has not been segregated into peripherally driven L-events and cortically generated H-events.…”

Section: Discussionsupporting

confidence: 78%

“…In summary, our framework for activity-dependent plasticity and receptive field refinement between thalamus and cortex with adaptive H-events can tune the properties of cortical spontaneous activity and provide a substrate for the event sparsification of cortical activity during development on a much longer timescale than receptive field refinement. This sparsification has been found in different sensory cortices, including visual [33], somatosensory [34] and auditory [57], suggesting a general principle that underlies network refinement. However, the event sparsification we observe is different than sparse network activity implicated in sparse efficient coding, which interestingly seems to decrease during development [59,60].…”

Section: Adaptive H-events Promote the Developmental Event Sparsificamentioning

confidence: 82%

“…Spontaneous activity is not static, but consists of distinct patterns that are dynamically regulated during development by ongoing activity-dependent plasticity which continuously reshapes network connectivity [33,34,57]. We next asked how our observed modifications in network connectivity that result in refined receptive fields based on fixed activity statistics during a single postnatal day might further modify spontaneous activity patterns on a much longer developmental timescale of several days.…”

Section: Adaptive H-events Promote the Developmental Event Sparsificamentioning

confidence: 99%

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Adaptation of spontaneous activity in the developing visual cortex

Wosniack

Kirchner

Chao

et al. 2020

Preprint

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Spontaneous activity drives the establishment of appropriate connectivity in different circuits during brain development. In the mouse primary visual cortex, two distinct patterns of spontaneous activity occur before vision onset: local low-synchronicity events originating in the retina, and global high-synchronicity events originating in the cortex. We sought to determine the contribution of these activity patterns to jointly organize network connectivity through different activity-dependent plasticity rules. We found that local events shape cortical input selectivity and topography, while global events have a homeostatic role regulating connection strength. To generate robust selectivity, we predicted that global events should adapt their amplitude to the history of preceding cortical activation, and confirmed by analyzing in vivo spontaneous cortical activity. This adaptation led to the sparsification of spontaneous activity on a slower timescale during development, demonstrating the remarkable capacity of the developing sensory cortex to acquire sensitivity to visual inputs after eye-opening.

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Section: Discussionsupporting

confidence: 78%

Section: Adaptive H-events Promote the Developmental Event Sparsificamentioning

confidence: 82%

Section: Adaptive H-events Promote the Developmental Event Sparsificamentioning

confidence: 99%

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Adaptation of spontaneous activity in the developing visual cortex

Wosniack

Kirchner

Chao

et al. 2020

Preprint

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“…We used numerical computer simulations to perform hypothetical experiments where we perturbed various parameters of the circuit model and observed the resulting changes in circuit-level activity. Although we focused on this particular brain circuit for tractability, our general conclusions and methodology should be readily applicable to other brain circuits ( Frye and MacLean, 2016 ).…”

Section: Resultsmentioning

confidence: 99%

Beyond excitation/inhibition imbalance in multidimensional models of neural circuit changes in brain disorders

O’Donnell

Gonçalves

Portera‐Cailliau

et al. 2017

eLife

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A leading theory holds that neurodevelopmental brain disorders arise from imbalances in excitatory and inhibitory (E/I) brain circuitry. However, it is unclear whether this one-dimensional model is rich enough to capture the multiple neural circuit alterations underlying brain disorders. Here, we combined computational simulations with analysis of in vivo two-photon Ca2+ imaging data from somatosensory cortex of Fmr1 knock-out (KO) mice, a model of Fragile-X Syndrome, to test the E/I imbalance theory. We found that: (1) The E/I imbalance model cannot account for joint alterations in the observed neural firing rates and correlations; (2) Neural circuit function is vastly more sensitive to changes in some cellular components over others; (3) The direction of circuit alterations in Fmr1 KO mice changes across development. These findings suggest that the basic E/I imbalance model should be updated to higher dimensional models that can better capture the multidimensional computational functions of neural circuits.

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“…Although we focus on this particular circuit for tractability, our general conclusions and 83 methodology should be readily applicable to other brain circuits (Frye and Maclean, 2016). 84…”

mentioning

confidence: 99%

Beyond excitation/inhibition imbalance in multidimensional models of neural circuit changes in brain disorders

O’Donnell

Gonçalves

Portera‐Cailliau

et al. 2016

Preprint

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13A leading theory holds that neurodevelopmental brain disorders arise from imbalances in 14 excitatory and inhibitory (E/I) brain circuitry. However, it is unclear whether this one-15 dimensional model is rich enough to capture the multiple neural circuit alterations 16 underlying brain disorders. Here we combined computational simulations with analysis of in 17 vivo 2-photon Ca 2+ imaging data from somatosensory cortex of Fmr1 knock-out (KO) mice, a 18 model of Fragile-X Syndrome, to test the E/I imbalance theory. We found that: 1) The E/I 19 imbalance model cannot account for joint alterations in the observed neural firing rates and 20 correlations; 2) Neural circuit function is vastly more sensitive to changes in some cellular 21 components over others; 3) The direction of circuit alterations in Fmr1 KO mice changes 22 across development. These findings suggest that the basic E/I imbalance model should be 23 updated to higher-dimensional models that can better capture the multidimensional 24 computational functions of neural circuits. 25. CC-BY-NC-ND 4.0 International license It is made available under a was not peer-reviewed) is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity.The copyright holder for this preprint (which . http://dx.doi.org/10.1101/086363 doi: bioRxiv preprint first posted online Nov. 7, 2016; O'Donnell et al.2

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Spontaneous activations follow a common developmental course across primary sensory areas in mouse neocortex

Abstract: Frye CG, MacLean JN. Spontaneous activations follow a common developmental course across primary sensory areas in mouse neocortex.

Cited by 14 publications

References 42 publications

Adaptation of spontaneous activity in the developing visual cortex

Adaptation of spontaneous activity in the developing visual cortex

Beyond excitation/inhibition imbalance in multidimensional models of neural circuit changes in brain disorders

Beyond excitation/inhibition imbalance in multidimensional models of neural circuit changes in brain disorders

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