Calcium entry through acetylcholine-channels can activate potassium conductance in bullfrog sympathetic neurons.
Fast B neurons in bullfrog sympathetic ganglia were voltage clamped with two microelectrodes. Acetylcholine (ACh) was applied onto the soma membrane by iontophoresis. A rapid nicotinic inward current was followed by a slow muscarinic inward current. After an addition of scopolamine to Ringer solution so as to block the muscarinic current, the nicotinic inward current was found to be followed by an outward current lasting for several hundred ms. It disappeared when the preceding nicotinic inward current was blocked by (+)-tubocurarine. The ACh-induced outward current was due to calcium entry through ACh-channels and subsequent opening of potassium channels. This may indicate that a rapid excitatory transmission leads to non-synaptic autoinhibition. The interaction between the calcium-dependent potassium conductance and the muscarinic action of ACh is proposed.
D000109:Acetylcholine / Q000378:metabolism*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D004553:Electric Conductivity; D005728:Ganglia, Sympathetic / Q000502:physiology*; D007473:Ion Channels / Q000378:metabolism*; D009474:Neurons / Q000502:physiology; D011188:Potassium / Q000502:physiology*; D011892:Rana catesbeiana; D012601:Scopolamine / Q000494:pharmacology; D014403:Tubocurarine / Q000494:pharmacology
D007473:Ion Channels; D012601:Scopolamine; D000109:Acetylcholine; D011188:Potassium; D002118:Calcium; D014403:Tubocurarine