Coding strategy for surface luminance switches in the primary visual cortex of the awake monkey

Both surface luminance and edge contrast of an object are essential features for object identification. However, cortical processing of surface luminance remains unclear. In this study, we aim to understand how the primary visual cortex (V1) processes surface luminance information across its different layers. We report that edge-driven responses are stronger than surface-driven responses in V1 input layers, but luminance information is coded more accurately by surface responses. In V1 output layers, the advantage of edge over surface responses increased eight times and luminance information was coded more accurately at edges. Further analysis of neural dynamics shows that such substantial changes for neural responses and luminance coding are mainly due to non-local cortical inhibition in V1’s output layers. Our results suggest that non-local cortical inhibition modulates the responses elicited by the surfaces and edges of objects, and that switching the coding strategy in V1 promotes efficient coding for luminance.

Parallel Advantage: Further Evidence for Bottom-up Saliency Computation by Human Primary Visual Cortex

Finding a target among uniformly oriented non-targets is typically faster when this target is perpendicular, rather than parallel, to the non-targets. The V1 Saliency Hypothesis (V1SH), that neurons in the primary visual cortex (V1) signal saliency for exogenous attentional attraction, predicts exactly the opposite in a special case: each target or non-target comprises two equally sized disks displaced from each other by 1.2 disk diameters center-to-center along a line defining its orientation. A target has two white or two black disks. Each non-target has one white disk and one black disk, and thus, unlike the target, activates V1 neurons less when its orientation is parallel rather than perpendicular to the neurons’ preferred orientations. When the target is parallel, rather than perpendicular, to the uniformly oriented non-targets, the target’s evoked V1 response escapes V1’s iso-orientation surround suppression, making the target more salient. I present behavioral observations confirming this prediction.

Multiple gamma rhythms carry distinct spatial frequency information in primary visual cortex

Gamma rhythms in many brain regions, including the primary visual cortex (V1), are thought to play a role in information processing. Here, we report a surprising finding of 3 narrowband gamma rhythms in V1 that processed distinct spatial frequency (SF) signals and had different neural origins. The low gamma (LG; 25 to 40 Hz) rhythm was generated at the V1 superficial layer and preferred a higher SF compared with spike activity, whereas both the medium gamma (MG; 40 to 65 Hz), generated at the cortical level, and the high gamma HG; (65 to 85 Hz), originated precortically, preferred lower SF information. Furthermore, compared with the rates of spike activity, the powers of the 3 gammas had better performance in discriminating the edge and surface of simple objects. These findings suggest that gamma rhythms reflect the neural dynamics of neural circuitries that process different SF information in the visual system, which may be crucial for multiplexing SF information and synchronizing different features of an object.

V1 encodes the perceived position of static but not moving objects

Brain activity in retinotopic cortex reflects illusory changes in stimulus position. Is this neural signature a general code for apparent position? Here we show that responses in primary visual cortex (V1) are consistent with perception of the Muller-Lyer illusion; however, we found no such signature for another striking illusion, the curveball effect. This demonstrates that V1 does not encode apparent position per se.

A Neurodynamic Model of Saliency Prediction in V1

Lateral connections in the primary visual cortex (V1) have long been hypothesized to be responsible for several visual processing mechanisms such as brightness induction, chromatic induction, visual discomfort, and bottom-up visual attention (also named saliency). Many computational models have been developed to independently predict these and other visual processes, but no computational model has been able to reproduce all of them simultaneously. In this work, we show that a biologically plausible computational model of lateral interactions of V1 is able to simultaneously predict saliency and all the aforementioned visual processes. Our model's architecture (NSWAM) is based on Penacchio's neurodynamic model of lateral connections of V1. It is defined as a network of firing rate neurons, sensitive to visual features such as brightness, color, orientation, and scale. We tested NSWAM saliency predictions using images from several eye tracking data sets. We show that the accuracy of predictions obtained by our architecture, using shuffled metrics, is similar to other state-of-the-art computational methods, particularly with synthetic images (CAT2000-Pattern and SID4VAM) that mainly contain low-level features. Moreover, we outperform other biologically inspired saliency models that are specifically designed to exclusively reproduce saliency. We show that our biologically plausible model of lateral connections can simultaneously explain different visual processes present in V1 (without applying any type of training or optimization and keeping the same parameterization for all the visual processes). This can be useful for the definition of a unified architecture of the primary visual cortex.

Sensory coding and contrast invariance emerge from the control of plastic inhibition over emergent selectivity

Visual stimuli are represented by a highly efficient code in the primary visual cortex, but the development of this code is still unclear. Two distinct factors control coding efficiency: Representational efficiency, which is determined by neuronal tuning diversity, and metabolic efficiency, which is influenced by neuronal gain. How these determinants of coding efficiency are shaped during development, supported by excitatory and inhibitory plasticity, is only partially understood. We investigate a fully plastic spiking network of the primary visual cortex, building on phenomenological plasticity rules. Our results suggest that inhibitory plasticity is key to the emergence of tuning diversity and accurate input encoding. We show that inhibitory feedback (random and specific) increases the metabolic efficiency by implementing a gain control mechanism. Interestingly, this led to the spontaneous emergence of contrast-invariant tuning curves. Our findings highlight that (1) interneuron plasticity is key to the development of tuning diversity and (2) that efficient sensory representations are an emergent property of the resulting network.

Closing the Critical Period Is Required for the Maturation of Binocular Integration in Mouse Primary Visual Cortex

Binocular matching of orientation preference between the two eyes is a common form of binocular integration that is regarded as the basis for stereopsis. How critical period plasticity enables binocular matching under the guidance of normal visual experience has not been fully demonstrated. To investigate how critical period closure affects the binocular matching, a critical period prolonged mouse model was constructed through the administration of bumetanide, an NKCC1 transporter antagonist. Using acute in vivo extracellular recording and molecular assay, we revealed that binocular matching was transiently disrupted due to heightened plasticity after the normal critical period, together with an increase in the density of spines and synapses, and the upregulation of GluA1 expression. Diazepam (DZ)/[(R, S)-3-(2-carboxypiperazin-4-yl) propyl-1-phosphonic acid (CPP)] could reclose the extended critical period, and rescue the deficits in binocular matching. Furthermore, the extended critical period, alone, with normal visual experience is sufficient for the completion of binocular matching in amblyopic mice. Similarly, prolonging the critical period into adulthood by knocking out Nogo-66 receptor can prevent the normal maturation of binocular matching and depth perception. These results suggest that maintaining an optimal plasticity level during adolescence is most beneficial for the systemic maturation. Extending the critical period provides new clues for the maturation of binocular vision and may have critical implications for the treatment of amblyopia.