TRPC channels regulate Ca2+-signaling and short-term plasticity of fast glutamatergic synapses

• Verfasst von: Schwarz, Yvonne [VerfasserIn]
• Verfasst von: Freichel, Marc [VerfasserIn]
• Titel: TRPC channels regulate Ca2+-signaling and short-term plasticity of fast glutamatergic synapses
• Verf.angabe: Yvonne Schwarz, Katharina Oleinikov, Barbara Schindeldecker, Amanda Wyatt, Petra Weißgerber, Veit Flockerzi, Ulrich Boehm, Marc Freichel, Dieter Bruns
• E-Jahr: 2019
• Jahr: September 19, 2019
• Umfang: 31 S.
• Fussnoten: Gesehen am 23.03.2020 ; Im Haupttitel ist "2+" hochgestellt
• Titel Quelle: Enthalten in: Public Library of SciencePLoS biology
• Ort Quelle: Lawrence, KS : PLoS, 2003
• Jahr Quelle: 2019
• Band/Heft Quelle: 17(2019,9) Artikel-Nummer e3000445, 31 Seiten
• ISSN Quelle: 1545-7885
• DOI: doi:10.1371/journal.pbio.3000445
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Depression
• Sach-SW: Neuronal plasticity
• Sach-SW: Neurons
• Sach-SW: Receptor potentials
• Sach-SW: Synapses
• Sach-SW: Synaptic plasticity
• Sach-SW: Transient receptor potential channels
• Sach-SW: Vesicles
• K10plus-PPN: 1693142600

Abstract

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.