Cortical Loops
cortical loops
Flexible motor sequence generation by thalamic control of cortical dynamics through low-rank connectivity perturbations
One of the fundamental functions of the brain is to flexibly plan and control movement production at different timescales to efficiently shape structured behaviors. I will present a model that clarifies how these complex computations could be performed in the mammalian brain, with an emphasis on the learning of an extendable library of autonomous motor motifs and the flexible stringing of these motifs in motor sequences. To build this model, we took advantage of the fact that the anatomy of the circuits involved is well known. Our results show how these architectural constraints lead to a principled understanding of how strategically positioned plastic connections located within motif-specific thalamocortical loops can interact with cortical dynamics that are shared across motifs to create an efficient form of modularity. This occurs because the cortical dynamics can be controlled by the activation of as few as one thalamic unit, which induces a low-rank perturbation of the cortical connectivity, and significantly expands the range of outputs that the network can produce. Finally, our results show that transitions between any motifs can be facilitated by a specific thalamic population that participates in preparing cortex for the execution of the next motif. Taken together, our model sheds light on the neural network mechanisms that can generate flexible sequencing of varied motor motifs.
Cortical-subcortical loops in olfaction (thalamus missing)?
Corticocortical and thalamocortical loops contributing to whisker sensory perception
Coordination of thalamo-cortical loops and global motor-sensory-motor loops in perception
The developing visual brain – answers and questions
We will start our talk with a short video of our research, illustrating methods (some old and new) and findings that have provided our current understanding of how visual capabilities develop in infancy and early childhood. However, our research poses some outstanding questions. We will briefly discuss three issues, which are linked by a common focus on the development of visual attentional processing: (1) How do recurrent cortical loops contribute to development? Cortical selectivity (e.g., to orientation, motion, and binocular disparity) develops in the early months of life. However, these systems are not purely feedforward but depend on parallel pathways, with recurrent feedback loops playing a critical role. The development of diverse networks, particularly for motion processing, may explain changes in dynamic responses and resolve developmental data obtained with different methodologies. One possible role for these loops is in top-down attentional control of visual processing. (2) Why do hyperopic infants become strabismic (cross-eyes)? Binocular interaction is a particularly sensitive area of development. Standard clinical accounts suppose that long-sighted (hyperopic) refractive errors require accommodative effort, putting stress on the accommodation-convergence link that leads to its breakdown and strabismus. Our large-scale population screening studies of 9-month infants question this: hyperopic infants are at higher risk of strabismus and impaired vision (amblyopia and impaired attention) but these hyperopic infants often under- rather than over-accommodate. This poor accommodation may reflect poor early attention processing, possibly a ‘soft sign’ of subtle cerebral dysfunction. (3) What do many neurodevelopmental disorders have in common? Despite similar cognitive demands, global motion perception is much more impaired than global static form across diverse neurodevelopmental disorders including Down and Williams Syndromes, Fragile-X, Autism, children with premature birth and infants with perinatal brain injury. These deficits in motion processing are associated with deficits in other dorsal stream functions such as visuo-motor co-ordination and attentional control, a cluster we have called ‘dorsal stream vulnerability’. However, our neuroimaging measures related to motion coherence in typically developing children suggest that the critical areas for individual differences in global motion sensitivity are not early motion-processing areas such as V5/MT, but downstream parietal and frontal areas for decision processes on motion signals. Although these brain networks may also underlie attentional and visuo-motor deficits , we still do not know when and how these deficits differ across different disorders and between individual children. Answering these questions provide necessary steps, not only increasing our scientific understanding of human visual brain development, but also in designing appropriate interventions to help each child achieve their full potential.