Calcium-dependent hyperpolarizations in bullfrog sympathetic neurons.
Intracellular recordings were made from neurons in bullfrog sympathetic ganglia. Fast B and slow B neurons were identified and selected for the analysis [Dodd and Horn (1983) J. Physiol., Lond. 334, 255-269]. A single soma action potential was followed by a prolonged afterhyperpolarization lasting for several hundred ms up to 2 s. Part of the spike afterhyperpolarization was due to potassium conductance activation triggered by calcium entry during an action potential. Acetylcholine was directly applied onto the soma membrane by iontophoresis. A rapid nicotinic depolarization was followed by a slow muscarinic depolarization. The nicotinic depolarization was followed by a hyperpolarization when the muscarinic depolarization was blocked by scopolamine. This hyperpolarization was several mV in amplitude and from 1 to 10 s in duration. It disappeared when the preceding nicotinic depolarization was blocked by (+)-tubocurarine. A single fast excitatory postsynaptic potential was also followed by a hyperpolarization in the presence of scopolamine. The acetylcholine-induced hyperpolarization was due to potassium conductance activation triggered by calcium entry during the nicotinic depolarization. The present findings show that non-synaptic autoinhibition is operating in sympathetic neurons. In other words, a rapid nicotinic transmission leads to prolonged hyperpolarizations which are not mediated by any transmitters but are mediated by calcium.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology*; D002799:Cholinergic Fibers / Q000502:physiology; D005728:Ganglia, Sympathetic / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009474:Neurons / Q000502:physiology; D011892:Rana catesbeiana; D009435:Synaptic Transmission
D000109:Acetylcholine; D002118:Calcium