Repetitive magnetic stimulation induces plasticity of excitatory postsynapses 
on proximal dendrites of cultured mouse CA1 pyramidal neurons

Lenz, Maximilian; Platschek, Steffen; Priesemann, Viola; Becker, Denise; Willems, Laurent M.; Ziemann, Ulf; Deller, Thomas; Müller-Dahlhaus, Florian; Jedlicka, Peter; Vlachos, Andreas

doi:10.1007/s00429-014-0859-9

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Repetitive magnetic stimulation induces plasticity of excitatory postsynapses on proximal dendrites of cultured mouse CA1 pyramidal neurons

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Priesemann, Viola
Department of Nonlinear Dynamics, Max Planck Institute for Dynamics and Self-Organization, Max Planck Society;

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Citation

Lenz, M., Platschek, S., Priesemann, V., Becker, D., Willems, L. M., Ziemann, U., et al. (2014). Repetitive magnetic stimulation induces plasticity of excitatory postsynapses on proximal dendrites of cultured mouse CA1 pyramidal neurons. Brain Structure and Function, 1-15. doi:10.1007/s00429-014-0859-9.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0029-0F17-F

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 entorhinohippocampal 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.