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Status epilepticus enhances depotentiation after fully established LTP in an NMDAR-Dependent but GluN2B-independent manner

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dc.contributor.author Guli, Xiati
dc.contributor.author Tokay, Tursonjan
dc.contributor.author Kirschstein, Timo
dc.contributor.author Köhling, Rüdiger
dc.date.accessioned 2016-02-03T04:41:58Z
dc.date.available 2016-02-03T04:41:58Z
dc.date.issued 2015-11-15
dc.identifier.uri http://nur.nu.edu.kz/handle/123456789/1133
dc.description.abstract N-Methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) can be reversed by low-frequency stimulation (LFS) referred to as depotentiation (DP). We previously found GluN2B upregulated in CA1 neurons from post-status epilepticus (post-SE) tissue associated with an enhanced LTP. Here,we testedwhether LFS-inducedDP is also altered in pathologicalGluN2B upregulation. Although LTP was enhanced in post-SE tissue, LTP was significantly reversed in this tissue, but not in controls. We next tested the effect of the GluN2B subunit-specific blocker Ro 25-6981 (1 𝜇M) on LFS-DP. As expected, LFS had no effect on synaptic strength in the presence of the GluN2B blocker in control tissue. In marked contrast, LFS-DP was also attained in post-SE tissue indicating that GluN2B was obviously not involved in depotentiation. To test for NMDA receptor-dependence, we applied the NMDA receptor antagonist D-AP5 (50 𝜇M) prior to LFS and observed that DPwas abolished in both control and post- SE tissue confirming NMDA receptor involvement. These results indicate that control Schaffer collateral-CA1 synapses cannot be depotentiated after fully established LTP, but LFS was able to reverse LTP significantly in post-SE tissue. However, while LFS-DP clearly requiredNMDA receptor activation, GluN2B-containingNMDA receptors were not involved in this formof depotentiation ru_RU
dc.language.iso en ru_RU
dc.publisher Neural Plasticity ru_RU
dc.rights Attribution-NonCommercial-NoDerivs 3.0 United States *
dc.rights.uri http://creativecommons.org/licenses/by-nc-nd/3.0/us/ *
dc.subject N-Methyl-D-aspartate ru_RU
dc.subject Epilepticus ru_RU
dc.subject Epilepticus enhances depotentiation ru_RU
dc.subject Research Subject Categories::MEDICINE ru_RU
dc.title Status epilepticus enhances depotentiation after fully established LTP in an NMDAR-Dependent but GluN2B-independent manner ru_RU
dc.type Article ru_RU

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