TRPM4-dependent post-synaptic depolarization is essential for the induction of NMDA receptor-dependent LTP in CA1 hippocampal neurons
TRPM4 is a calcium-activated but calcium-impermeable non-selective cation (CAN) channel. Previous studies have shown that TRPM4 is an important regulator of Ca2+-dependent changes in membrane potential in excitable and non-excitable cell types. However, its physiological significance in neurons of t...
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| Main Authors: | , , , , , , , , , , , |
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| Format: | Article (Journal) |
| Language: | English |
| Published: |
2016
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| In: |
Pflügers Archiv
Year: 2015, Volume: 468, Issue: 4, Pages: 593-607 |
| ISSN: | 1432-2013 |
| DOI: | 10.1007/s00424-015-1764-7 |
| Online Access: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1007/s00424-015-1764-7
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| Author Notes: | Aurélie Menigoz, Tariq Ahmed, Victor Sabanov, Koenraad Philippaert, Silvia Pinto, Sara Kerselaers, Andrei Segal, Marc Freichel, Thomas Voets, Bernd Nilius, Rudi Vennekens, Detlef Balschun |
MARC
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| 245 | 1 | 0 | |a TRPM4-dependent post-synaptic depolarization is essential for the induction of NMDA receptor-dependent LTP in CA1 hippocampal neurons |c Aurélie Menigoz, Tariq Ahmed, Victor Sabanov, Koenraad Philippaert, Silvia Pinto, Sara Kerselaers, Andrei Segal, Marc Freichel, Thomas Voets, Bernd Nilius, Rudi Vennekens, Detlef Balschun |
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| 520 | |a TRPM4 is a calcium-activated but calcium-impermeable non-selective cation (CAN) channel. Previous studies have shown that TRPM4 is an important regulator of Ca2+-dependent changes in membrane potential in excitable and non-excitable cell types. However, its physiological significance in neurons of the central nervous system remained unclear. Here, we report that TRPM4 proteins form a CAN channel in CA1 neurons of the hippocampus and we show that TRPM4 is an essential co-activator of N-methyl-d-aspartate (NMDA) receptors (NMDAR) during the induction of long-term potentiation (LTP). Disrupting the Trpm4 gene in mice specifically eliminates NMDAR-dependent LTP, while basal synaptic transmission, short-term plasticity, and NMDAR-dependent long-term depression are unchanged. The induction of LTP in Trpm4−/−neurons was rescued by facilitating NMDA receptor activation or post-synaptic membrane depolarization. Accordingly, we obtained normal LTP in Trpm4−/−neurons in a pairing protocol, where post-synaptic depolarization was applied in parallel to pre-synaptic stimulation. Taken together, our data are consistent with a novel model of LTP induction in CA1 hippocampal neurons, in which TRPM4 is an essential player in a feed-forward loop that generates the post-synaptic membrane depolarization which is necessary to fully activate NMDA receptors during the induction of LTP but which is dispensable for the induction of long-term depression (LTD). These results have important implications for the understanding of the induction process of LTP and the development of nootropic medication. | ||
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| 700 | 1 | |a Ahmed, Tariq |e VerfasserIn |4 aut | |
| 700 | 1 | |a Sabanov, Victor |e VerfasserIn |4 aut | |
| 700 | 1 | |a Philippaert, Koenraad |e VerfasserIn |4 aut | |
| 700 | 1 | |a Pinto, Silvia |e VerfasserIn |4 aut | |
| 700 | 1 | |a Kerselaers, Sara |e VerfasserIn |4 aut | |
| 700 | 1 | |a Segal, Andrei |e VerfasserIn |4 aut | |
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| 700 | 1 | |a Voets, Thomas |e VerfasserIn |4 aut | |
| 700 | 1 | |a Nilius, Bernd |e VerfasserIn |4 aut | |
| 700 | 1 | |a Vennekens, Rudi |e VerfasserIn |4 aut | |
| 700 | 1 | |a Balschun, Detlef |e VerfasserIn |4 aut | |
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