Table of Contents Author Guidelines Submit a Manuscript
Neural Plasticity
Volume 2014 (2014), Article ID 684238, 8 pages
Research Article

NMDA Receptor-Dependent Metaplasticity by High-Frequency Magnetic Stimulation

1Oscar Langendorff Institute of Physiology, University of Rostock, Gertrudenstraße 9, 18057 Rostock, Germany
2Center for Life Sciences, Nazarbayev University, 53 Kabanbay Batyr Avenue, Astana 010000, Kazakhstan
3Institute of Sport Sciences, University of Rostock, Ulmenstraße 69, 18057 Rostock, Germany

Received 8 August 2014; Revised 30 September 2014; Accepted 1 October 2014; Published 28 October 2014

Academic Editor: George W. Huntley

Copyright © 2014 Tursonjan Tokay et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


High-frequency magnetic stimulation (HFMS) can elicit N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) at Schaffer collateral-CA1 pyramidal cell synapses. Here, we investigated the priming effect of HFMS on the subsequent magnitude of electrically induced LTP in the CA1 region of rat hippocampal slices using field excitatory postsynaptic potential (fEPSP) recordings. In control slices, electrical high-frequency conditioning stimulation (CS) could reliably induce LTP. In contrast, the same CS protocol resulted in long-term depression when HFMS was delivered to the slice 30 min prior to the electrical stimulation. HFMS-priming was diminished when applied in the presence of the metabotropic glutamate receptor antagonists (RS)-α-methylserine-O-phosphate (MSOP) and (RS)-α-methyl-4-carboxyphenylglycine (MCPG). Moreover, when HFMS was delivered in the presence of the NMDA receptor-antagonist D-2-amino-5-phosphonovalerate (50 µM), CS-induced electrical LTP was again as high as under control conditions in slices without priming. These results demonstrate that HFMS significantly reduced the propensity of subsequent electrical LTP and show that both metabotropic glutamate and NMDA receptor activation were involved in this form of HFMS-induced metaplasticity.