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Status Epilepticus Enhances Depotentiation after Fully Established LTP in an NMDAR-Dependent but GluN2B-Independent Manner
Joint Authors
Guli, Xiati
Köhling, Rüdiger
Kirschstein, Timo
Tokay, Tursonjan
Source
Issue
Vol. 2016, Issue 2016 (31 Dec. 2016), pp.1-10, 10 p.
Publisher
Hindawi Publishing Corporation
Publication Date
2016-01-03
Country of Publication
Egypt
No. of Pages
10
Main Subjects
Abstract EN
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 tested whether LFS-induced DP is also altered in pathological GluN2B 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 DP was 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 required NMDA receptor activation, GluN2B-containing NMDA receptors were not involved in this form of depotentiation.
American Psychological Association (APA)
Guli, Xiati& Tokay, Tursonjan& Kirschstein, Timo& Köhling, Rüdiger. 2016. Status Epilepticus Enhances Depotentiation after Fully Established LTP in an NMDAR-Dependent but GluN2B-Independent Manner. Neural Plasticity،Vol. 2016, no. 2016, pp.1-10.
https://search.emarefa.net/detail/BIM-1113233
Modern Language Association (MLA)
Guli, Xiati…[et al.]. Status Epilepticus Enhances Depotentiation after Fully Established LTP in an NMDAR-Dependent but GluN2B-Independent Manner. Neural Plasticity No. 2016 (2016), pp.1-10.
https://search.emarefa.net/detail/BIM-1113233
American Medical Association (AMA)
Guli, Xiati& Tokay, Tursonjan& Kirschstein, Timo& Köhling, Rüdiger. Status Epilepticus Enhances Depotentiation after Fully Established LTP in an NMDAR-Dependent but GluN2B-Independent Manner. Neural Plasticity. 2016. Vol. 2016, no. 2016, pp.1-10.
https://search.emarefa.net/detail/BIM-1113233
Data Type
Journal Articles
Language
English
Notes
Includes bibliographical references
Record ID
BIM-1113233