TRPC channels regulate Ca2+-signaling and short-term plasticity of fast glutamatergic synapses
Transient receptor potential (TRP) proteins form Ca2+-permeable, nonselective cation channels, but their role in neuronal Ca2+ homeostasis is elusive. In the present paper, we show that TRPC channels potently regulate synaptic plasticity by changing the presynaptic Ca2+-homeostasis of hippocampal ne...
Gespeichert in:
| Hauptverfasser: | , |
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| Dokumenttyp: | Article (Journal) |
| Sprache: | Englisch |
| Veröffentlicht: |
September 19, 2019
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| In: |
PLoS biology
Year: 2019, Jahrgang: 17, Heft: 9 |
| ISSN: | 1545-7885 |
| DOI: | 10.1371/journal.pbio.3000445 |
| Online-Zugang: | Verlag, lizenzpflichtig, Volltext: https://doi.org/10.1371/journal.pbio.3000445 Verlag, lizenzpflichtig, Volltext: https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.3000445 
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| Verfasserangaben: | Yvonne Schwarz, Katharina Oleinikov, Barbara Schindeldecker, Amanda Wyatt, Petra Weißgerber, Veit Flockerzi, Ulrich Boehm, Marc Freichel, Dieter Bruns |
MARC
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| 245 | 1 | 0 | |a TRPC channels regulate Ca2+-signaling and short-term plasticity of fast glutamatergic synapses |c Yvonne Schwarz, Katharina Oleinikov, Barbara Schindeldecker, Amanda Wyatt, Petra Weißgerber, Veit Flockerzi, Ulrich Boehm, Marc Freichel, Dieter Bruns |
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| 520 | |a Transient receptor potential (TRP) proteins form Ca2+-permeable, nonselective cation channels, but their role in neuronal Ca2+ homeostasis is elusive. In the present paper, we show that TRPC channels potently regulate synaptic plasticity by changing the presynaptic Ca2+-homeostasis of hippocampal neurons. Specifically, loss of TRPC1/C4/C5 channels decreases basal-evoked secretion, reduces the pool size of readily releasable vesicles, and accelerates synaptic depression during high-frequency stimulation (HFS). In contrast, primary TRPC5 channel-expressing neurons, identified by a novel TRPC5-τ-green fluorescent protein (τGFP) knockin mouse line, show strong short-term enhancement (STE) of synaptic signaling during HFS, indicating a key role of TRPC5 in short-term plasticity. Lentiviral expression of either TRPC1 or TRPC5 turns classic synaptic depression of wild-type neurons into STE, demonstrating that TRPCs are instrumental in regulating synaptic plasticity. Presynaptic Ca2+ imaging shows that TRPC activity strongly boosts synaptic Ca2+ dynamics, showing that TRPC channels provide an additional presynaptic Ca2+ entry pathway, which efficiently regulates synaptic strength and plasticity. | ||
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| 650 | 4 | |a Neuronal plasticity | |
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