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Galanis, C.

Publications and source records attributed to Galanis, C..

2 recordsLinked to original sources

Multi-scale Modeling Toolbox for Single Neuron and Subcellular Activity under (repetitive) Transcranial Magnetic Stimulation

Transcranial Magnetic Stimulation (TMS) is a non-invasive brain stimulation technique widely used in research and clinical applications. However, its mechanism of action and the neural response to TMS are still poorly understood. Multi-scale modeling can complement experimental research and provide a framework between the physical input parameters and the subcellular neural effects of TMS. At the macroscopic level, sophisticated numerical models exist to estimate the induced electric fields in whole-brain volume conductor models. However, multi-scale computational modeling approaches to predict TMS cellular and subcellular responses, crucial to understanding TMS plasticity inducing protocols, are not available so far. Here, we develop a multi-scale Neuron Modeling for TMS toolbox (NeMo-TMS) that enables researchers to easily generate accurate neuron models from morphological reconstructions, couple them to the external electric fields induced by TMS, and to simulate the cellular and subcellular responses of the neurons. Both single-pulse and rTMS protocols can be simulated and results visualized in 3D. We openly share our toolbox and provide example scripts and datasets for the user to explore. NeMo-TMS toolbox (https://github.com/OpitzLab/NeMo-TMS) allows researchers a previously not available level of detail and precision in realistically modeling the physical and physiological effects of TMS.

neuroscience

Amyloid-beta mediates homeostatic synaptic plasticity

The physiological role of the amyloid-precursor protein (APP) is insufficiently understood. Recent work has implicated APP in the regulation of synaptic plasticity. Substantial evidence exists for a role of APP and its secreted ectodomain APPs in Hebbian plasticity. Here, we addressed the relevance of APP in homeostatic synaptic plasticity using organotypic tissue cultures of APP-/- mice. In the absence of APP, dentate granule cells failed to strengthen their excitatory synapses homeostatically. Homeostatic plasticity is rescued by amyloid-{beta} (A{beta}) and not by APPs, and it is neither observed in APP+/+ tissue treated with {beta}- or {gamma}-secretase inhibitors nor in synaptopodin-deficient cultures lacking the Ca2+-dependent molecular machinery of the spine apparatus. Together, these results suggest a role of APP processing via the amyloidogenic pathway in homeostatic synaptic plasticity, representing a function of relevance for brain physiology as well as for brain states associated with increased A{beta} levels.

neuroscience