Repetitive magnetic stimulation induces plasticity of inhibitory synapses

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作者
Maximilian Lenz
Christos Galanis
Florian Müller-Dahlhaus
Alexander Opitz
Corette J. Wierenga
Gábor Szabó
Ulf Ziemann
Thomas Deller
Klaus Funke
Andreas Vlachos
机构
[1] Institute of Clinical Neuroanatomy,Department of Neurology and Stroke and Hertie Institute for Clinical Brain Research
[2] Neuroscience Center,Division of Cell Biology
[3] Goethe-University,Department of Neurophysiology
[4] Eberhard-Karls-University,undefined
[5] Center for Biomedical Imaging and Neuromodulation,undefined
[6] Nathan Kline Institute for Psychiatric Research,undefined
[7] Orangeburg,undefined
[8] New York 10962,undefined
[9] USA,undefined
[10] Center for the Developing Brain,undefined
[11] Child Mind Institute,undefined
[12] New York,undefined
[13] New York 10022,undefined
[14] USA,undefined
[15] Faculty of Science,undefined
[16] Utrecht University,undefined
[17] Laboratory of Molecular Biology and Genetics,undefined
[18] Institute of Experimental Medicine,undefined
[19] Medical Faculty,undefined
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摘要
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.
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