GABAergic function and dysfunction in visual perception

Thursday, October 28, 12:00 – 14:00 ET // Register here

This session has already occurred. You can watch a replay here.

A series of studies in human subjects over the last 10 years have advanced the idea that there are individual differences in GABA concentration in human occipital cortex, and that these individual differences are related to differences in visual perception via suppressive mechanisms. Moreover, there is evidence that neuropsychiatric abnormalities (ASD, schizophrenia, and depression) are associated with alterations in GABA tone and perception. This session reviews psychophysical and MRI spectroscopic measurements putatively related to GABA function in people with neuropsychiatric disorders and in a neurotypical population.

This special session is being hosted by the Clinical Vision Sciences Technical Group and the Vision Technical Group along with the Fall Vision Meeting Planning Committee.

Invited Speakers:

• Steven Dakin, University of Auckland

• Scott Murray, University of Washington

• Caroline E. Robertson, Dartmouth College

• Duje Tadin, University of Rochester

Moderators:

• Geoff Aguirre, University of Pennsylvania

• Holly Bridge, John Radcliffe Hospital

Abstracts:

Abnormal processing of visual context in schizophrenia

Steven C. Dakin, School of Optometry and Vision Science, The University of Auckland, Aotearoa New Zealand; UCL Institute of Ophthalmology, University College London, UK

People with schizophrenia (SZ) exhibit persistent deficits in visual processing including reduced contrast sensitivity and poor detection of complex image structure, such as contours. Over recent years accumulating psychophysical evidence indicates that vision in SZ is associated with a reduced influence of spatial context which in turn has been attributed to reduced spatial suppression in visual cortex. Compared to controls, people with SZ do not experience the same reduction in perceived contrast that occurs when targets are embedded in a high contrast background. This appears to be a cortical phenomenon: reduced influence of context is not limited to contrast but carries over to other image attributes (such as orientation) but not others (such as luminance). Finally, although patients poor processing of higher-order image structure has been attributed to differences in perceptual grouping, work from my lab indicates that abnormal processing of context may also contribute to patients’ poor sensitivity for contours. It does this by (a) reducing their sensitivity to local orientation and (b) reducing their ability to discount irrelevant background structure. Taken together these results suggest that abnormal processing of context contributes to a range of visual processing deficits in SZ.

Funding Acknowledgement: Funded by the Wellcome Trust.

Visual suppression and inhibition are not the same thing

Scott Murray, Department of Psychology, University of Washington

Visual suppression is an experimental finding of a reduction in behavioral performance or a reduction in neural response that occurs when a visual stimulus is surrounded by other visual stimuli. This reduction is typically attributed to neural inhibition. Understanding the link between visual suppression and neural inhibition is important because suppression is frequently used to infer the integrity of inhibitory neural circuits in conditions such as autism, schizophrenia, depression, ageing, and others. Using pharmacology, spectroscopy, fMRI, and computational modeling, I will discuss evidence from our lab that questions whether neural inhibition is the main contributor to visual suppression.

Funding Acknowledgement: NIH R01 MH106520.

Sensory processing in autism – Translational markers and circuit-level insights

Caroline Robertson, Department of Psychological and Brain Sciences, Dartmouth College, Hanover, NH USA

Atypical sensory experience is estimated to occur in as many as 90% of autistic individuals and to affect every sensory modality: taste, touch, audition, olfaction and vision. Because the neural computations underlying sensory processing are relatively well understood in typically developing individuals and are conserved between humans and other animals, sensory paradigms have considerable potential for shedding light on autistic neurobiology. But are sensory traits, in fact, core phenotypic markers of autism? In this talk, I will argue that the answer is “yes” . The evidence I review shows that the autistic cortex is affected by distinct, low-level changes in neural circuitry that is dedicated to perceptual processing (including primary sensory areas). Further, perceptual symptoms in individuals with autism are evident early in development, account for independent variance in diagnostic criteria of the condition, and show a persistent relationship to clinical measures of higher-order social cognition and behavior. Finally, I will present data from a recent line of work in my laboratory using behavioral, neuroimaging, pharmacological techniques to identify a marker of autism in low-level visual processing, which has provided concrete insight into the neurobiology of autism in humans.

Strong evidence against a common center-surround mechanism in visual processing

Duje Tadin, Brain & Cognitive Sciences, Center for Visual Science, Ophthalmology, and Neuroscience, University of Rochester

Events and objects in the world generally do not occur in isolation. This surrounding spatial and temporal information has major effects on visual processing, effects that are typically described as contextual modulations. Given qualitative similarities among various contextual surround effects (e.g., the effects tend to exaggerate differences and suppress uniform stimuli), it might seem intuitive that these processes are related. It is unknown, however, whether contextual modulation processes across visual sub-modalities are independent, or at least in part share a common underlying mechanism. This is especially relevant for clinical work where these contextual effects are often linked to inhibitory function.

We addressed this question using an individual differences approach in three different populations (total N = 129): neurotypical adults, older adults and patients with schizophrenia. The context battery included six tasks that assessed surround modulations in luminance, contrast, orientation, motion (2X) and size domains.

The results revealed robust contextual effects across all tasks. However, despite large sample sizes, we found no significant correlations among different contextual tasks. Across groups, we did find significant differences: (a) weaker surround contrast effect in both schizophrenia and older adults, (b) stronger repulsive surround tilt and motion effects in older adults and (c) weaker surround suppression for motion in both schizophrenia and older adults.

We find that (1) strength of contextual modulation does not correlate across visual sub-modalities and (2) deficits in contextual modulation that go in different directions. Together, this indicates an absence of a common underlying mechanism for contextual modulation in vision.