scholarly journals Regulation of spike timing in visual cortical circuits

2008 ◽  
Vol 9 (2) ◽  
pp. 97-107 ◽  
Author(s):  
Paul Tiesinga ◽  
Jean-Marc Fellous ◽  
Terrence J. Sejnowski
Keyword(s):  
Spike Timing ◽  
Cortical Circuits ◽  
Visual Cortical

scholarly journals Routing information flow by separate neural synchrony frequencies allows for “functionally labeled lines” in higher primate cortex

2019 ◽  
Vol 116 (25) ◽  
pp. 12506-12515 ◽  
Author(s):  
Mohammad Bagher Khamechian ◽  
Vladislav Kozyrev ◽  
Stefan Treue ◽  
Moein Esghaei ◽  
Mohammad Reza Daliri
Keyword(s):  
Information Flow ◽  
Information Transfer ◽  
Sensory Information ◽  
Spike Timing ◽  
Oscillatory Activity ◽  
Attention Task ◽  
Cortical Areas ◽  
High Gamma ◽  
Ventral Pathway ◽  
Visual Cortical

Efficient transfer of sensory information to higher (motor or associative) areas in primate visual cortical areas is crucial for transforming sensory input into behavioral actions. Dynamically increasing the level of coordination between single neurons has been suggested as an important contributor to this efficiency. We propose that differences between the functional coordination in different visual pathways might be used to unambiguously identify the source of input to the higher areas, ensuring a proper routing of the information flow. Here we determined the level of coordination between neurons in area MT in macaque visual cortex in a visual attention task via the strength of synchronization between the neurons’ spike timing relative to the phase of oscillatory activities in local field potentials. In contrast to reports on the ventral visual pathway, we observed the synchrony of spikes only in the range of high gamma (180 to 220 Hz), rather than gamma (40 to 70 Hz) (as reported previously) to predict the animal’s reaction speed. This supports a mechanistic role of the phase of high-gamma oscillatory activity in dynamically modulating the efficiency of neuronal information transfer. In addition, for inputs to higher cortical areas converging from the dorsal and ventral pathway, the distinct frequency bands of these inputs can be leveraged to preserve the identity of the input source. In this way source-specific oscillatory activity in primate cortex can serve to establish and maintain “functionally labeled lines” for dynamically adjusting cortical information transfer and multiplexing converging sensory signals.

Effects of Spike Timing on Winner-Take-All Competition in Model Cortical Circuits

2000 ◽  
Vol 12 (1) ◽  
pp. 181-194 ◽  
Author(s):  
Erik D. Lumer
Keyword(s):  
Action Potentials ◽  
Spike Timing ◽  
Neuronal Responses ◽  
Cortical Circuits ◽  
Cortical Tissue ◽  
Motor Action ◽  
Recurrent Excitation ◽  
Synaptic Interactions ◽  
Winner Take All ◽  
Take All

Synaptic interactions in cortical circuits involve strong recurrent excitation between nearby neurons and lateral inhibition that is more widely spread. This architecture is commonly thought to promote a winner-takeall competition, in which a small fraction of neuronal responses is selected for further processing. Here I report that such a competition is remarkably sensitive to the timing of neuronal action potentials. This is shown using simulations of model neurons and synaptic connections representing a patch of cortical tissue. In the simulations, uncorrelated discharge among neuronal units results in patterns of response dominance and suppression, that is, in a winner-take-all competition. Synchronization of firing, however, prevents such competition. These results demonstrate a novel property of recurrent cortical-like circuits, suggesting that the temporal patterning of cortical activity may play an important part in selection among stimuli competing for the control of attention and motor action.

scholarly journals Visual Cortex Engagement in Retinitis Pigmentosa

2021 ◽  
Vol 22 (17) ◽  
pp. 9412
Author(s):  
Gianluca Pietra ◽  
Tiziana Bonifacino ◽  
Davide Talamonti ◽  
Giambattista Bonanno ◽  
Alessandro Sale ◽  
...  
Keyword(s):  
Visual Cortex ◽  
Retinitis Pigmentosa ◽  
Intracortical Inhibition ◽  
Visual Sensitivity ◽  
Cortical Circuits ◽  
Inherited Disorders ◽  
Progressive Degeneration ◽  
Visual Inputs ◽  
Retinal Photoreceptors ◽  
Visual Cortical

Retinitis pigmentosa (RP) is a family of inherited disorders caused by the progressive degeneration of retinal photoreceptors. There is no cure for RP, but recent research advances have provided promising results from many clinical trials. All these therapeutic strategies are focused on preserving existing photoreceptors or substituting light-responsive elements. Vision recovery, however, strongly relies on the anatomical and functional integrity of the visual system beyond photoreceptors. Although the retinal structure and optic pathway are substantially preserved at least in early stages of RP, studies describing the visual cortex status are missing. Using a well-established mouse model of RP, we analyzed the response of visual cortical circuits to the progressive degeneration of photoreceptors. We demonstrated that the visual cortex goes through a transient and previously undescribed alteration in the local excitation/inhibition balance, with a net shift towards increased intracortical inhibition leading to improved filtering and decoding of corrupted visual inputs. These results suggest a compensatory action of the visual cortex that increases the range of residual visual sensitivity in RP.

scholarly journals Rapid learning in visual cortical networks

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Ye Wang ◽  
Valentin Dragoi
Keyword(s):  
Brain Activity ◽  
Local Population ◽  
Low Frequency ◽  
Spike Timing ◽  
Learning Performance ◽  
Cell Populations ◽  
Frequency Synchronization ◽  
Population Activity ◽  
Area V4 ◽  
Visual Cortical

Although changes in brain activity during learning have been extensively examined at the single neuron level, the coding strategies employed by cell populations remain mysterious. We examined cell populations in macaque area V4 during a rapid form of perceptual learning that emerges within tens of minutes. Multiple single units and LFP responses were recorded as monkeys improved their performance in an image discrimination task. We show that the increase in behavioral performance during learning is predicted by a tight coordination of spike timing with local population activity. More spike-LFP theta synchronization is correlated with higher learning performance, while high-frequency synchronization is unrelated with changes in performance, but these changes were absent once learning had stabilized and stimuli became familiar, or in the absence of learning. These findings reveal a novel mechanism of plasticity in visual cortex by which elevated low-frequency synchronization between individual neurons and local population activity accompanies the improvement in performance during learning.

A Calcium-Based Simple Model of Multiple Spike Interactions in Spike-Timing-Dependent Plasticity

2013 ◽  
Vol 25 (7) ◽  
pp. 1853-1869 ◽  
Author(s):  
Takumi Uramoto ◽  
Hiroyuki Torikai
Keyword(s):  
Synaptic Weight ◽  
Spike Timing ◽  
State Variables ◽  
Spike Timing Dependent Plasticity ◽  
Dependent Plasticity ◽  
Synaptic Modification ◽  
Proposed Model ◽  
Layer 2 ◽  
Visual Cortical ◽  
Cortical Slices

Spike-timing-dependent plasticity (STDP) is a form of synaptic modification that depends on the relative timings of presynaptic and postsynaptic spikes. In this letter, we proposed a calcium-based simple STDP model, described by an ordinary differential equation having only three state variables: one represents the density of intracellular calcium, one represents a fraction of open state NMDARs, and one represents the synaptic weight. We shown that in spite of its simplicity, the model can reproduce the properties of the plasticity that have been experimentally measured in various brain areas (e.g., layer 2/3 and 5 visual cortical slices, hippocampal cultures, and layer 2/3 somatosensory cortical slices) with respect to various patterns of presynaptic and postsynaptic spikes. In addition, comparisons with other STDP models are made, and the significance and advantages of the proposed model are discussed.

Fast synchronization of perceptual grouping in laminar visual cortical circuits

2004 ◽  
Vol 17 (5-6) ◽  
pp. 707-718 ◽  
Author(s):  
Arash Yazdanbakhsh ◽  
Stephen Grossberg
Keyword(s):  
Perceptual Grouping ◽  
Cortical Circuits ◽  
Visual Cortical

scholarly journals Syngap1 Dynamically Regulates the Fine-Scale Reorganization of Cortical Circuits in Response to Sensory Experience

2020 ◽  
Author(s):  
Nerea Llamosas ◽  
Thomas Vaissiere ◽  
Camilo Rojas ◽  
Sheldon Michaelson ◽  
Courtney A. Miller ◽  
...  
Keyword(s):  
Neurodevelopmental Disorders ◽  
Cortical Plasticity ◽  
Neurodevelopmental Disorder ◽  
Spike Timing ◽  
Sensory Cortex ◽  
Fine Scale ◽  
Cortical Circuits ◽  
Population Activity ◽  
Cellular Processes

AbstractExperience induces complex, neuron-specific changes in population activity within sensory cortex circuits. However, the mechanisms that enable neuron-specific changes within cortical populations remain unclear. To explore the idea that synapse strengthening is involved, we studied fine-scale cortical plasticity in Syngap1 mice, a neurodevelopmental disorder model useful for linking synapse biology to circuit functions. Repeated functional imaging of the same L2/3 somatosensory cortex neurons during single whisker experience revealed that Syngap1 selectively regulated the plasticity of a low-active, or “silent”, neuronal subpopulation. Syngap1 also regulated spike-timing-dependent synaptic potentiation and experience-mediated in vivo synapse bouton formation, but not synaptic depression or bouton elimination in L2/3. Adult re-expression of Syngap1 restored plasticity of “silent” neurons, demonstrating that this gene controls dynamic cellular processes required for population-specific changes to cortical circuits during experience. These findings suggest that abnormal experience-dependent redistribution of cortical population activity may contribute to the etiology of neurodevelopmental disorders.

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