Tokimasa T
Neuroscience. 1984 Jul;12(3):929-37. doi: 10.1016/0306-4522(84)90180-5.
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.
