| Literature DB >> 25108309 |
Maximilian Lenz1, Steffen Platschek1, Viola Priesemann2,3, Denise Becker1, Laurent M Willems1, Ulf Ziemann4, Thomas Deller1, Florian Müller-Dahlhaus4, Peter Jedlicka1, Andreas Vlachos5.
Abstract
Repetitive transcranial magnetic stimulation (rTMS) of the human brain can lead to long-lasting changes in cortical excitability. However, the cellular and molecular mechanisms which underlie rTMS-induced plasticity remain incompletely understood. Here, we used repetitive magnetic stimulation (rMS) of mouse entorhino-hippocampal slice cultures to study rMS-induced plasticity of excitatory postsynapses. By employing whole-cell patch-clamp recordings of CA1 pyramidal neurons, local electrical stimulations, immunostainings for the glutamate receptor subunit GluA1 and compartmental modeling, we found evidence for a preferential potentiation of excitatory synapses on proximal dendrites of CA1 neurons (2-4 h after stimulation). This rMS-induced synaptic potentiation required the activation of voltage-gated sodium channels, L-type voltage-gated calcium channels and N-methyl-D-aspartate-receptors. In view of these findings we propose a cellular model for the preferential strengthening of excitatory synapses on proximal dendrites following rMS in vitro, which is based on a cooperative effect of synaptic glutamatergic transmission and postsynaptic depolarization.Entities:
Keywords: 3D-reconstruction; AMPA-receptors; Backpropagating action potentials; Computational modelling; Hebbian plasticity; Silent synapses; Spike timing dependent plasticity; Strontium
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Year: 2014 PMID: 25108309 DOI: 10.1007/s00429-014-0859-9
Source DB: PubMed Journal: Brain Struct Funct ISSN: 1863-2653 Impact factor: 3.270