Repetitive magnetic stimulation induces plasticity of inhibitory synapses

Maximilian Lenz, Christos Galanis, Florian Müller-Dahlhaus, Alexander Opitz, Corette J. Wierenga, Gábor Szabó, Ulf Ziemann, Thomas Deller, Klaus Funke and Andreas Vlachos ()
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Maximilian Lenz: Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University
Christos Galanis: Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University
Florian Müller-Dahlhaus: Eberhard-Karls-University
Alexander Opitz: Center for Biomedical Imaging and Neuromodulation, Nathan Kline Institute for Psychiatric Research, Orangeburg, New York 10962, USA
Corette J. Wierenga: Faculty of Science, Utrecht University
Gábor Szabó: Laboratory of Molecular Biology and Genetics, Institute of Experimental Medicine
Ulf Ziemann: Eberhard-Karls-University
Thomas Deller: Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University
Klaus Funke: Medical Faculty
Andreas Vlachos: Institute of Clinical Neuroanatomy, Neuroscience Center, Goethe-University

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract Repetitive transcranial magnetic stimulation (rTMS) is used as a therapeutic tool in neurology and psychiatry. While repetitive magnetic stimulation (rMS) has been shown to induce plasticity of excitatory synapses, it is unclear whether rMS can also modify structural and functional properties of inhibitory inputs. Here we employed 10-Hz rMS of entorhinohippocampal slice cultures to study plasticity of inhibitory neurotransmission on CA1 pyramidal neurons. Our experiments reveal a rMS-induced reduction in GABAergic synaptic strength (2–4 h after stimulation), which is Ca2+-dependent and accompanied by the remodelling of postsynaptic gephyrin scaffolds. Furthermore, we present evidence that 10-Hz rMS predominantly acts on dendritic, but not somatic inhibition. Consistent with this finding, a reduction in clustered gephyrin is detected in CA1 stratum radiatum of rTMS-treated anaesthetized mice. These results disclose that rTMS induces coordinated Ca2+-dependent structural and functional changes of specific inhibitory postsynapses on principal neurons.

Date: 2016
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DOI: 10.1038/ncomms10020

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