Seminario: "Cortical layer with no known function" (Prof. Zoltan Molnar)
Seminario de investigación "Cortical layer with no known function"
Ponente: Prof. Zoltan Molnar, Dept. of Physiology, Anatomy and Genetics, Univ. de Oxford, Inglaterra
Fecha y hora: Viernes 29 de abril de 2016, a las 13:00 horas
Lugar: Aula 0 de la Facultad de Medicina de la UAM.
Zoltán Molnár MD DPhil
Professor of Developmental Neuroscience
Department of Physiology, Anatomy and Genetics
University of Oxford, South Parks Road, Oxford, OX1 3QX, UK
http://www.dpag.ox.ac.uk/team/zoltan-molnar
CORTICAL LAYER WITH NO KNOWN FUNCTION
How do we distinguish the stimuli reaching us from the external world from our own imagination; our planned from our actual movements? Our brain collects sensory information from the outside world and it compares our own plans with our actual movements. The structure that orchestrates these sensory and motor functions is the thalamus. The thalamus has two functionally distinct sets of nuclei. Strong peripheral sensory inputs target first-order thalamic nuclei and these relay information to the cerebral cortex. Projections from the cortical layer 6 innervate all thalamic nuclei. They provide numerous, but weak input to both thalamic relay cells in first-order nuclei, and higher-order thalamic nuclei. This input is termed “modulatory”. The layer 5 cortico-thalamic projections provide sparse but powerful input to cells exclusively in higher-order thalamic nuclei. This input is termed “driver” input and mediates trans-thalamic cortico-cortical relays. We wish to study the relationship and development of cortico-thalamic projections and test the hypothesis that a transient cell population that is normally only present during early cortical development, the subplate (Hoerder-Suabedissen and Molnár, 2015) provide driver or modulator input to the thalamus in rodents. We examine the rearrangement of the projections to first and higher order thalamic nuclei (cross-hierarchical cortico-thalamic plasticity) after alterations of the sensory periphery, when sensory driver input to first-order nuclei is lost (Grant et al., 2016). This form of plasticity has not been considered in the development of normal cortical arealisation or cognitive disorders. Additionally, we study normal and pathological development of the mouse and human cerebral cortex with special attention to the interstitial white matter cells (remnants of subplate neurons) that have been associated with schizophrenia (Hoerder-Suabedissen et al., 2013), a cognitive disorder where the distinctions between the external stimuli and imagination are disrupted.