Multiple components of surround modulation in primary visual cortex: Multiple neural circuits with multiple functions?

Responses of many neurons in primary visual cortex (V1) are suppressed by stimuli exceeding the classical receptive field (RF), an important property that might underlie the computation of visual saliency. Traditionally, it has proven difficult to disentangle the underlying neural circuits, including feedforward, horizontal intracortical, and feedback connectivity. Since circuit-level analysis is particularly feasible in the mouse, we asked whether neural signatures of spatial integration in mouse V1 are similar to those of higher-order mammals and investigated the role of parvalbumin-expressing (PV+) inhibitory interneurons. Analogous to what is known from primates and carnivores, we demonstrate that, in awake mice, surround suppression is present in the majority of V1 neurons and is strongest in superficial cortical layers. Anesthesia with isoflurane-urethane, however, profoundly affects spatial integration: it reduces the laminar dependency, decreases overall suppression strength, and alters the temporal dynamics of responses. We show that these effects of brain state can be parsimoniously explained by assuming that anesthesia affects contrast normalization. Hence, the full impact of suppressive influences in mouse V1 cannot be studied under anesthesia with isoflurane-urethane. To assess the neural circuits of spatial integration, we targeted PV+ interneurons using optogenetics. Optogenetic depolarization of PV+ interneurons was associated with increased RF size and decreased suppression in the recorded population, similar to effects of lowering stimulus contrast, suggesting that PV+ interneurons contribute to spatial integration by affecting overall stimulus drive. We conclude that the mouse is a promising model for circuit-level mechanisms of spatial integration, which relies on the combined activity of different types of inhibitory interneurons.

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Sensory experience during locomotion promotes recovery of function in adult visual cortex

eLife ◽

10.7554/elife.02798 ◽

2014 ◽

Vol 3 ◽

Cited By ~ 53

Author(s):

Megumi Kaneko ◽

Michael P Stryker

Keyword(s):

Visual Cortex ◽

Primary Visual Cortex ◽

Neural Circuits ◽

Visual Stimulation ◽

Recovery Of Function ◽

Sensory Deprivation ◽

Sensory Experience ◽

Inhibitory Neurons ◽

Visual Responses ◽

Effective Stimulus

Recovery from sensory deprivation is slow and incomplete in adult visual cortex. In this study, we show that visual stimulation during locomotion, which increases the gain of visual responses in primary visual cortex, dramatically enhances recovery in the mouse. Excitatory neurons regained normal levels of response, while narrow-spiking (inhibitory) neurons remained less active. Visual stimulation or locomotion alone did not enhance recovery. Responses to the particular visual stimuli viewed by the animal during locomotion recovered, while those to another normally effective stimulus did not, suggesting that locomotion promotes the recovery only of the neural circuits that are activated concurrent with the locomotion. These findings may provide an avenue for improving recovery from amblyopia in humans.

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Optimal compensation for neuron death

10.1101/029512 ◽

2015 ◽

Cited By ~ 2

Author(s):

David Barrett ◽

Sophie Deneve ◽

Christian Machens

Keyword(s):

Synaptic Plasticity ◽

Visual Cortex ◽

Primary Visual Cortex ◽

Neural Circuits ◽

Brain Lesions ◽

Compensatory Mechanism ◽

Neuron Death ◽

Tuning Curves ◽

Neural Damage ◽

The Brain

The brain has an impressive ability to withstand neural damage. Diseases that kill neurons can go unnoticed for years, and incomplete brain lesions or silencing of neurons often fail to produce any effect. How does the brain compensate for such damage, and what are the limits of this compensation? We propose that neural circuits optimally compensate for neuron death, thereby preserving their function as much as possible. We show that this compensation can explain changes in tuning curves induced by neuron silencing across a variety of systems, including the primary visual cortex. We find that optimal compensation can be implemented through the dynamics of networks with a tight balance of excitation and inhibition, without requiring synaptic plasticity. The limits of this compensatory mechanism are reached when excitation and inhibition become unbalanced, thereby demarcating a recovery boundary, where signal representation fails and where diseases may become symptomatic.

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Excitatory and inhibitory L2/3 neurons in mouse primary visual cortex are balanced in their input connectivity

10.1101/2020.04.21.053504 ◽

2020 ◽

Author(s):

Alexander P.Y. Brown ◽

Lee Cossell ◽

Troy W. Margrie

Keyword(s):

Visual Cortex ◽

Long Range ◽

Primary Visual Cortex ◽

Analytical Approach ◽

Neural Circuits ◽

Brain Regions ◽

Inhibitory Neurons ◽

Hierarchical Segmentation ◽

Layer 2 ◽

Inhibitory Networks

AbstractQuantitatively characterising brain-wide connectivity of neural circuits is of vital importance in understanding the function of the mammalian cortex. Here we have designed an analytical approach to examine data from hierarchical segmentation ontologies, and applied it in the comparison of long-range presynaptic connectivity onto excitatory and inhibitory neurons in layer 2/3 (L2/3) of mouse primary visual cortex (V1). We find that long-range connections onto these two general cell classes in L2/3 originate from highly similar brain regions, and in similar proportions, when compared to input to layer 6. These anatomical data suggest that distal information received by excitatory and inhibitory networks is highly homogenous in L2/3.

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