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Features of maladaptive reorganization of canonical circuits underlying cortical malformation induced sensory and cognitive deficits

Journal of Neurology & Neurophysiology

ISSN - 2155-9562

Features of maladaptive reorganization of canonical circuits underlying cortical malformation induced sensory and cognitive deficits

Joint Event on 23rd International Conference on Neurology & Neurophysiology & 24th International Conference on Neurosurgery and Neuroscience

March 18-19, 2019 Edinburgh, Scotland

Qian-Quan Sun, Weiguo Yang and Anthony Williams

University of Wyoming, USA

Posters & Accepted Abstracts: J Neurol Neurophysiol

Abstract :

Malformation of cortical development underlies a significant portion of intellectual and cognitive deficits and intractable epilepsy in human patients. How aberrant synapses of cortical elements contribute to sensory and cognitive deficits remains unclear. Our recent results demonstrate inputs and layer, and cell type specific features of E/I balance. Building on this study, the goal of this study is to understand how canonical cortical circuits in the barrel cortex are maladaptively wired and if the knowledge of this maladaptive wiring helps the understanding of sensory deficits, cognitive problems and epileptiform activities in vivo. Our comprehensive mapping studies identified a hot spot: the L2/3 but not L5B excitatory pyramidal cells (PCs), located far away (~1 mm) from the microgyrus, form maladaptive hyperexcitable circuits that involves de novo inter-laminar and intercolumnar but not intracolumnar excitatory inputs. Functions of somatostatin interneurons were impaired in a layer-specific fashion, consistent with its contribution to the altered excitabilities. Second, combining optogenetic manipulation and multi-electrode array and EEG recordings, we found that this ‚??hot spot‚?? are responsible for the up-state and epileptiform activities under both optogenetic, and whisker-stimulation under light anesthesia. We conclude that sensory and cognitive deficits in this model results from overabundant excitatory innervation in a layer, region and cell-type specific fashion, leading to imbalanced excitation and inhibition. The imbalanced cortical activities may be triggered by the thalamocortical inputs during normal sensory process, and slow wave sleep period, resulting in sensory deficits during awake and spike-wave-discharges during sleep.

Biography :

Qian-Quan Sun has completed his PhD from Andrews University and Postdoctoral studies from Stanford University School of Medicine. He is the Director of Wyoming Sensory Biology Center, a NIH funded center of biomedicla excellence. He has published 40 papers in peer reviewed journals.

E-mail: [email protected]

 

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