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TRPC channels regulate Ca2+-signaling and short-term plasticity of fast glutamatergic synapses.
- Source :
- PLoS Biology; 9/19/2019, Vol. 17 Issue 9, p1-31, 31p, 8 Graphs
- Publication Year :
- 2019
-
Abstract
- Transient receptor potential (TRP) proteins form Ca<superscript>2+</superscript>-permeable, nonselective cation channels, but their role in neuronal Ca<superscript>2+</superscript> homeostasis is elusive. In the present paper, we show that TRPC channels potently regulate synaptic plasticity by changing the presynaptic Ca<superscript>2+</superscript>-homeostasis of hippocampal neurons. Specifically, loss of TRPC1/C4/C5 channels decreases basal-evoked secretion, decreases 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 Ca<superscript>2+</superscript> imaging shows that TRPC activity strongly boosts synaptic Ca<superscript>2+</superscript> dynamics, showing that TRPC channels provide an additional presynaptic Ca<superscript>2+</superscript> entry pathway, which efficiently regulates synaptic strength and plasticity. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 15449173
- Volume :
- 17
- Issue :
- 9
- Database :
- Complementary Index
- Journal :
- PLoS Biology
- Publication Type :
- Academic Journal
- Accession number :
- 138707758
- Full Text :
- https://doi.org/10.1371/journal.pbio.3000445