Abstract

Intracellular recordings were made from ‘fast B’ [9] neurons in bullfrog sympathetic ganglia. A single soma action potential was followed by a prolonged after-hyperpolarization lasting for several hundred milliseconds up to 2 s. The spike afterhyperpolarization, which is generated by calcium-dependent potassium conductance increase (g KCa) [3,20–24], was shortened by the muscarinic action of acetylcholine and oxotremorine (30–300 nM). These concentrations of muscarinic agonists were too low to cause any detectable changes in resting membrane potential, input resistance or action potential wave form. ACh released from presynaptic terminal under a physiological condition also caused the shortening of the calciumdependent hyperpolarization. The results suggested that the shortening of calciumdependent spike afterhyperpolarization may permit the neuron to pass the high frequency of discharge during the muscarinic excitation.

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