To block muscle stimulation μ-conotoxin GIIIB (#C-270, Alomone Labs Ltd, Jerusalem, Israel) was used. This toxin inhibits sarcolemmal voltage-dependent sodium channels (VSDCs) without affecting synaptic ACh release or ACh signaling [42 (link)]. It was supplied as lyophilized powder of > 99% purity. μ-conotoxin GIIIB was 150 μM stock, and working concentration was 1.5 μM in Ringer’s solution [mM: NaCl 137, KCl 5, CaCl2 2, MgSO4 1, NaH2PO4 1, NaHCO3 12, glucose 12.1, and DMSO 0.1%, oxygenated with O2:CO2 (95:5)].
PKA activity was blocked with N-[2-((p-Bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89, Calbiochem). H-89 was made as 10 mM stock and used at 10 μM diluted in Ringer’s solution with DMSO.
All chemicals were diluted in Ringer’s solution, and both control and drug-containing solutions contained 0.1% dimethyl sulfoxide (DMSO) as the vehicle.
PKA activity was blocked with N-[2-((p-Bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide dihydrochloride (H-89, Calbiochem). H-89 was made as 10 mM stock and used at 10 μM diluted in Ringer’s solution with DMSO.
All chemicals were diluted in Ringer’s solution, and both control and drug-containing solutions contained 0.1% dimethyl sulfoxide (DMSO) as the vehicle.
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