Topographic representation of the sensory space in the brain is essential for sensory information processing and perception. The somatosensory and motor cortical maps in each hemisphere represent the contralateral body and the face. This is due to midline crossing of the ascending (sensory) and descending (motor) pathways at the level of the medulla or the pons. Genetic and developmental defects in midline crossing or injury at the crossing site severely affect sensory-motor information processing and actions in both animals and humans. In this proposal we use a region-specific gene deletion mouse model to study the consequences of partial crossing of the ascending somatosensory face pathway. Midline crossing defects in this mouse leads to bilateral face representation in the thalamus and subsequently in the somatosensory cortex. We will use this mouse model to investigate (a) morphological and electrophysiological properties of the pre and postsynaptic elements in the """"""""bifacial"""""""" cortical map;(b) altered thalamocortical and corticocortical connectivity patterns in response to bilateral face representation;(c) behavioral consequences of this genetic mutation. A combination of molecular, morphological, electrophysiological, voltage-sensitive dye imaging and behavioral techniques will be used to elucidate mechanisms underlying the functional organization and behavioral manifestations of developmental injury-related or genetic defects in ascending somatosensory pathways.

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Perception of body and face sensations occurs through information processing in neural maps formed by somatosensory pathways of the brain. In particular, the neocortex has a disproportionate map of the face and body, which reflects the density of sensory receptors in the periphery. Sensory maps of each brain hemisphere process information from the opposite side of the body. Developmental injury or congenital defects in somatosensory pathways result in abnormal map formation. We will investigate the functional and behavioral consequences of such a map defect in a transgenic mouse model with duplicated face maps in each brain hemisphere.

National Institute of Health (NIH)
National Institute of Neurological Disorders and Stroke (NINDS)
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Special Emphasis Panel (ZRG1)
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Gnadt, James W
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University of Maryland Baltimore
Anatomy/Cell Biology
Schools of Medicine
United States
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