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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

Memory deficits are a debilitating symptom of epilepsy, but little is known about mechanisms underlying cognitive deficits. Here, we describe a Na+ channel-dependent mechanism underlying altered hippocampal dendritic integration, degraded place coding, and deficits in spatial memory. Two-photon glutamate uncaging experiments

An inhibitory extracellular milieu and neuron-intrinsic processes prevent axons from regenerating in the adult central nervous system (CNS). Here we show how the two aspects are interwoven. Genetic loss-of-function experiments determine that the small GTPase RhoA relays extracellular inhibitory signals to the cytoskeleton by adapting mechanisms

We are happy and excited to announce that the DFG has  extended funding for the CRC 1089 for another 4 years. In the CRC 1089, BCN scientists together with partners from the DZNE and caesar, as well as national and

Bonn/Germany, October 31, 2019. During embryonic development, nerve cells form thin, long extensions, which they use to wire up a complex network, the brain. Scientists from the German Center for Neurodegenerative Diseases (DZNE) in Bonn have now identified a protein

SFB1089 member Prof. Bradke, who works at the German Center for Neurodegenerative Diseases (DZNE) and his group have identified a group of proteins that help to regenerate damaged nerve cells. Their findings are reported in the journal “Neuron”. It is

Bonn/Geneva, January, 30th, 2019.  Frank Bradke, a senior researcher at the German Center for Neurodegenerative Diseases (DZNE) and a professor at the University of Bonn, will be awarded the Roger de Spoelberch Prize, which is endowed with 750,000 euros. The Swiss Roger