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Inflammation and Synaptic Plasticity

A major hallmark of brain diseases is neuroinflammation. We are interested in how immune mediators affect synaptic plasticity. Particularly, our work focuses on better understanding how these factors influence intracellular calcium stores, i.e. the spine apparatus organelle, and how these changes alter the ability of neurons to express associative and homeostatic synaptic plasticity. We study the role of coagulation factors in this context and test whether these changes can be modified by rTMS.

 

Ben Shimon M*, Lenz M*, Ikenberg B, Becker D, Shavit Stein E, Chapmann J, Tanne D, Pick CG, Blatt I, Neufeld M, Vlachos A*, Maggio N*° (2015) Thrombin regulation of synaptic transmission and plasticity: implications for health and disease. Front Cel Neurosci. 9: 151.

Becker D, Deller T, Vlachos A° (2015) Tumor necrosis factor (TNF)-receptor 1 and 2 mediate homeostatic synaptic plasticity of denervated mouse dentate granule cells. Sci Rep. 5: 12726.

Strehl A, Lenz M, Itsekson-Hayosh Z, Becker D, Chapman J, Deller T, Maggio N, Vlachos A° (2014) Systemic inflammation is associated with a reduction in Synaptopodin expression in the mouse hippocampus. Exp Neurol. 261: 230-235.

Becker D, Zahn D, Deller T, Vlachos A° (2013) Tumor necrosis factor alpha maintains denervation-induced homeostatic synaptic plasticity of mouse dentate granule cells. Front Cell Neurosci. 7: 257.