Stimulus-dependent delay of perceptual filling-in by microsaccades.

Perception is a function of both stimulus features and active sensory sampling. The illusion of perceptual filling-in occurs when eye gaze is kept still: visual boundary perception may fail, causing adjacent visual features to remarkably merge into one uniform visual surface. Microsaccades-small, involuntary eye movements during gaze fixation-counteract perceptual filling-in, but the mechanisms underlying this process are not well understood. We investigated whether microsaccade efficacy for preventing filling-in depends on two boundary properties, color contrast and retinal eccentricity (distance from gaze center). Twenty-one human participants (male and female) fixated on a point until they experienced filling-in between two isoluminant colored surfaces. We found that increased color contrast independently extends the duration before filling-in but does not alter the impact of individual microsaccades. Conversely, lower eccentricity delayed filling-in only by increasing microsaccade efficacy. We propose that microsaccades facilitate stable boundary perception via a transient retinal motion signal that scales with eccentricity but is invariant to boundary contrast. These results shed light on how incessant eye movements integrate with ongoing stimulus processing to stabilize perceptual detail, with implications for visual rehabilitation and the optimization of visual presentations in virtual and augmented reality environments.

Network mechanisms of ongoing brain activity's influence on conscious visual perception.

Sensory inputs enter a constantly active brain, whose state is always changing from one moment to the next. Currently, little is known about how ongoing, spontaneous brain activity participates in online task processing. We employed 7 Tesla fMRI and a threshold-level visual perception task to probe the effects of prestimulus ongoing brain activity on perceptual decision-making and conscious recognition. Prestimulus activity originating from distributed brain regions, including visual cortices and regions of the default-mode and cingulo-opercular networks, exerted a diverse set of effects on the sensitivity and criterion of conscious recognition, and categorization performance. We further elucidate the mechanisms underlying these behavioral effects, revealing how prestimulus activity modulates multiple aspects of stimulus processing in highly specific and network-dependent manners. These findings reveal heretofore unknown network mechanisms underlying ongoing brain activity's influence on conscious perception, and may hold implications for understanding the precise roles of spontaneous activity in other brain functions.

Perceptual filling-in dispels the veridicality problem of conscious perception research.

Conscious perceptual experiences are expected to correlate with content-specific brain activity. A veridicality problem arises when attempting to disentangle unconscious and conscious brain processes if conscious perceptual contents accurately match the physical nature of the stimulus. We argue that perceptual filling-in, a phenomenon whereby visual information inaccurately spreads across visual space, is a promising approach to circumvent the veridicality problem. Filling-in generates non-veridical although unambiguous percepts dissociated from stimulus input. In particular, the radial uniformity illusion induces a filling-in experience between a central disk and the surrounding periphery. We discuss how this illusion facilitates both the detection of neurophysiological responses and subjective phenomenological monitoring. We report behavioral effects from a large-sample (n = 200) psychophysics study and examine key stimulus parameters that drive the conscious filling-in experience. We propose that these data underpin future hypothesis-driven studies of filling-in to further delineate the neural mechanisms of conscious perception.

Cortical and subcortical signatures of conscious object recognition.

The neural mechanisms underlying conscious recognition remain unclear, particularly the roles played by the prefrontal cortex, deactivated brain areas and subcortical regions. We investigated neural activity during conscious object recognition using 7 Tesla fMRI while human participants viewed object images presented at liminal contrasts. Here, we show both recognized and unrecognized images recruit widely distributed cortical and subcortical regions; however, recognized images elicit enhanced activation of visual, frontoparietal, and subcortical networks and stronger deactivation of the default-mode network. For recognized images, object category information can be decoded from all of the involved cortical networks but not from subcortical regions. Phase-scrambled images trigger strong involvement of inferior frontal junction, anterior cingulate cortex and default-mode network, implicating these regions in inferential processing under increased uncertainty. Our results indicate that content-specific activity in both activated and deactivated cortical networks and non-content-specific subcortical activity support conscious recognition.

Context-dependent odor learning requires the anterior olfactory nucleus.

Learning to associate the context in which a stimulus occurs is an important aspect of animal learning. We propose that the association of an olfactory stimulus with its multisensory context is mediated by projections from ventral hippocampus (vHC) networks to the anterior olfactory nucleus (AON). Using a contextually cued olfactory discrimination task, rats were trained to associate 2 olfactory stimuli with different responses depending on visuospatial context. Temporary lesions of the AON or vHC impaired performance on this task. In contrast, such lesions did not impair performance on a noncontextual olfactory discrimination task. Moreover, vHC lesions also impaired performance on an analogous contextually cued texture discrimination task, whereas AON lesions affected only olfactory contextual associations. We describe a distinct role for the AON in olfactory processing and conclude that early olfactory networks such as the olfactory bulb and AON function as multimodal integration networks rather than processing olfactory signals exclusively. (PsycInfo Database Record (c) 2020 APA, all rights reserved).

α-Tubulin Acetyltransferase Is a Novel Target Mediating Neurite Growth Inhibitory Effects of Chondroitin Sulfate Proteoglycans and Myelin-Associated Glycoprotein.

Damage to the CNS results in neuronal and axonal degeneration, and subsequent neurological dysfunction. Endogenous repair in the CNS is impeded by inhibitory chemical and physical barriers, such as chondroitin sulfate proteoglycans (CSPGs) and myelin-associated glycoprotein (MAG), which prevent axon regeneration. Previously, it has been demonstrated that the inhibition of axonal histone deacetylase-6 (HDAC6) can promote microtubule α-tubulin acetylation and restore the growth of CSPGs- and MAG-inhibited axons. Since the acetylation of α-tubulin is regulated by two opposing enzymes, HDAC6 (deacetylation) and α-tubulin acetyltransferase-1 (αTAT1; acetylation), we have investigated the regulation of these enzymes downstream of a growth inhibitory signal. Our findings show that exposure of primary mouse cortical neurons to soluble CSPGs and MAG substrates cause an acute and RhoA-kinase-dependent reduction in α-tubulin acetylation and αTAT1 protein levels, without changes to either HDAC6 levels or HDAC6 activity. The CSPGs- and MAG-induced reduction in αTAT1 occurs primarily in the distal and middle regions of neurites and reconstitution of αTAT1, either by Rho-associated kinase (ROCK) inhibition or lentiviral-mediated αTAT1 overexpression, can restore neurite growth. Lastly, we demonstrate that CSPGs and MAG signaling decreases αTAT1 levels posttranscriptionally via a ROCK-dependent increase in αTAT1 protein turnover. Together, these findings define αTAT1 as a novel potential therapeutic target for ameliorating CNS injury characterized by growth inhibitory substrates that are prohibitive to axonal regeneration.