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• W2951036656 endingPage "116567" @default.
• W2951036656 startingPage "116567" @default.
• W2951036656 abstract "Metabotropic glutamate receptor 5 (mGluR5), a member of group I mGluR, exerts its effect via elevation of intracellular Ca 2+ level. We here characterized Ca 2+ signals in the tsA201 cells transfected with mGluR5 and investigated the role of passages for mGluR5-induced Ca 2+ signals in synaptic plasticity. Using a genetically encoded Ca 2+ indicator, GCamp2, Ca 2+ signals were reliably induced by bath application of ( S )-3,5-dihydroxyphenylglycine, the group I mGluR agonist, in the tsA201 cells transfected with mGluR5. Using whole-cell recordings in the substantia gelatinosa (SG) neurons of the spinal trigeminal subnucleus caudalis (Vc), excitatory postsynaptic currents were recorded by stimulating the trigeminal tract. Ca 2+ signals were mediated by “classical” or “canonical” transient receptor potential (TRPC) channels, particularly TRPC1/3/4/6, but not TRPC5, naturally existing in the tsA201 cells. Interestingly, the induction of Ca 2+ signals was independent of the phospholipase C signaling pathway; instead, it critically involves the cyclic adenosine diphosphate ribose/ryanodine receptor-dependent signaling pathway and only partially protein kinase C. On the other hand, both TRPC3 and TRPC4 mediated mGluR1/5-induced long-lasting potentiation of excitatory synaptic transmission from the trigeminal primary afferents to the SG neurons of the Vc. This study demonstrates that endogenous TRPC channels contribute to mGluR5-induced Ca 2+ signals in tsA201 cells and synaptic plasticity at excitatory synapses." @default.
• W2951036656 created "2019-06-27" @default.
• W2951036656 creator A5011388700 @default.
• W2951036656 creator A5025834667 @default.
• W2951036656 date "2019-08-01" @default.
• W2951036656 modified "2023-09-27" @default.
• W2951036656 title "Endogenous TRPC channels mediate Ca2+ signals and trigeminal synaptic plasticity induced by mGluR5" @default.
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• W2951036656 doi "https://doi.org/10.1016/j.lfs.2019.116567" @default.
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