A study led by the IEECR has identified a mechanism relying on Ste20-like kinase that allows single cortical neurons to cell-autonomously adjust feedforward inhibition they receive to the cell-specific levels of excitatory input. The authors propose that this mechanism is critical to ensure that a majority of cortical pyramidal cells participate in information coding. A collaborative study performed with our collaborators from the German Center for Neurodegenerative Diseases and the Max Planck Institute for Neurobiology of Behavior.
The results have now been published in the journal Cell Reports. Please follow this to find out more