Multiple studies suggest that schizophrenia, dyslexia and autism are sensory disorders that show deficits in visual perceptual processing at different levels of the visual system, from primary visual cortex to higher-order extrastriate visual cortex. These deficits have been related to changes in the functioning of the magnocellular-(M-) visual pathway. The magnocellular system conducts low-resolution visual information rapidly to cortex, and is involved in attentional capture and processing of overall stimulus organization. I propose studying circuit mechanisms of visual information processing that maybe underlie these visual perceptual symptoms by using molecular and anatomical techniques. By developing a new approach to studying specific anatomical circuits -- in V1 in normal and dysfunctional brains -- I anticipate the method will be able to be generalized to other cortical areas thereby establishing a general model for the study of specific circuit abnormalities in human brain. In the proposal I will focus in the human layer 4Cα of V1, which is the main thalamic recipient layer. If there are perceptual deficits in the M-pathway I suggest that there would be structural brain changes that could lead to these impairments. Previously it has been described that there was a reduction in the number of neurons in V1, but I propose to quantify specifically the number of neurons in 4Cα to test the hypothesis that there should be an implication of this layer in the deficit of the M-pathway. But I will not only focus on studying the density of neurons, I will also study their morphological arborizations and their dendritic spine density. I will quantify the number of thalamic afferents that neurons in 4Cα receive in the brains of normal and schizophrenic individuals, to determine whether M-pathway is affected at the level of thalamic afferent. Later I will go one step further in the M-pathway to study the projections from 4Cα neurons to 4B neurons, which are a key element in the M-pathway as they project to MT. Recently we have observed that some 4B neurons express a specific subunit of potassium channel, Kv3.1b, which give them the ability to have narrow spike widths that could fire sequences of spikes at high rates without accommodating, which is important if there are processing motion information. If in schizophrenia there is a deficit in motion processing, I propose that these fast-spiking neurons could be affected in these perceptual disorders. The second main goal of this proposal would be to identify these neurons in human, study their distribution and co-expression with other markers for interneurons or excitatory neurons and observe how these neurons are distributed in dysfunctional brains. Overall my goal is to find morphological brain changes that could explain the deficits in visual perceptual processing.