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The KCl application caused membrane depolarization, and as a consequence, opening of voltage-dependent calcium channels.
A representative experiment of a cortical neuron expressing tdTA is shown in Figure 3. Perfusion with high K+ buffer produced membrane depolarization, the opening of voltage-dependent Ca2+ channels, Ca2+ entry and a bioluminescent tdTA response (Figure 3A).
This results in the opening of voltage-dependent Ca2+ channels.
This causes membrane depolarization and the opening of voltage-dependent Ca2+ channels.
EC coupling is activated by an incoming action potential wavefront and the subsequent opening of voltage-dependent L-type Ca2+ channels (CaV1.2).
Voltage-gated K+ (KV) channels are known effector proteins which are inhibited by hypoxia, leading to cell membrane depolarization and opening of voltage-dependent L-type Ca2+ channels.
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Interestingly, the 5IA85380-evoked GABA overflow was abolished in the presence of TTX, demonstrating that opening of voltage dependent sodium channels is required for the α4β2 nAChR effect to occur.
The exposure to K+(>30 mM) can induce contraction of smooth muscles through opening of voltage dependent calcium channels, increased influx of extracellular Ca+2 leading to contractile effect [ 50].
These 'presteady-state or gating currents' precede the opening and closing of voltage-dependent channels.
Mitiglinide, a derivative of benzylsuccinic acid, closes adenosine triphosphate-dependent K+ channels by selectively binding to the SU receptor on pancreatic β-cells, which leads to opening of the voltage-dependent calcium channels and induces insulin secretion.
This hyperpolarisation of the smooth muscle cells will decrease the opening of the voltage-dependent Ca2+ channels and would be expected therefore to reduce the Ca2+ signal produced in coronary arterial myocytes by agonists working through this pathway, i.e. stimulating Ca2+ entry.
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