Modulation of synaptic plasticity after trauma (A02)

• Subject Area: Molecular Biology and Physiology of Neurons and Glial Cells
• Term: since 2015
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 251293561

We have analyzed synaptic dynamics and plasticity after trauma: A peripheral trauma (TXT) causes a significant reduction of synapses (and structural changes of mitochondria) in the hippocampus that could be responsible for a delirium-like state. The loss of synapses is caused by local CRH release and BDNF reduction within the hippocampus. The molecular pathways downstream from CRH receptor 1 leading to these structural alterations are different. TBI causes the loss of hippocampal synapses at the injury site as well as at the contralateral site within a week after injury. Synapses lacking isoforms of the scaffolding molecule Shank3 display only a slight reduction of excitatory synapses and no morphological signs of synaptic plasticity after TBI. Therefore, we aim to elucidate the CRH receptor 1-dependent signaling cascades in hippocampal neurons and the mechanisms that cause a plastic vs. a “non-plastic” Shank3 KO brain after injury.

• DFG Programme: Collaborative Research Centres
• Subproject of: SFB 1149: Danger Response, Disturbance Factors and Regenerative Potential after Acute Trauma
• Applicant Institution: Universität Ulm
• Project Head: Professor Dr. Tobias Böckers