The role of neural activity in wiring and plasticity of sensory pathways is a major topic of interest in developmental neuroscience. During the past decade, considerable attention is directed toward the role of N-methyl D Aspartate (NMDA) receptor-mediated neural activity. There is a vast body of literature that underscores the importance of NMDA receptors during development of neural connections and their plasticity, learning and memory, as well as during excitotoxicity in pathological states of the mature nervous system in many species, including the primates. This proposal focuses on the development and plasticity of neural connections along the somatosensory pathway in mice with genetic manipulations of the NMDA receptor function. Rodent somatosensory pathway is an excellent model system to study development of topographic connections and patterning within somatosensory maps. Previous studies found that in mice lacking the critical subunit of the NMDA receptors, somatosensory patterns are abolished in the brainstem. Mice that express lower levels of NMDA receptor function also show absence of patterning all along the somatosensory pathway conveying information from the face region. The long term objective of this proposal is to reveal how cellular elements such as axon arbors and dendritic processes of postsynaptic cells are altered following impaired NMDA receptor function. A combined molecular genetic and neuroanatomical approach will be used to elucidate structural changes along the somatosensory pathway of these mice. A clear understanding of such anatomical changes will pave the way for dissecting out molecular mechanisms of pattern formation and plasticity in developing mammalian sensory pathways.
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