Abstract
In the paravertebral sympathetic chain of bullfrogs, some part of the preganglionic nerve located within the ganglion was depolarized transiently when acetylcholine (ACh) was directly applied to the ganglion, particularly in the presence of an anticholinesterase (anti-ChE). The axonal part of the preganglionic nerve, on the other hand, showed no detectable depolarization following direct application of ACh (with anti-ChEs) to the interganglionic nerve trunk. The ACh depolarization was markedly depressed by nicotine, and less markedly by (+)-tubocurarine, whereas it was not affected by atropine. Nicotine, similar to ACh, transiently depolarized only the intraganglionic portion of the presynaptic fibers. The action potentials, recorded from the axonal as well as the terminal parts of the preganglionic nerve, showed spike potentials followed by a marked negative after-potential. The negative after-potential was followed by a positive after-potential which was markedly enhanced by repetitive nerve stimulation. A slow negative potential followed the positive after-potential in the repetitive responses of the terminal parts of the preganglionic nerve. The slow negative potential was enhanced by anti-ChEs, eliminated by ACh and nicotine, and unaffected by atropine. The amplitude of the action potentials of the terminal parts of the preganglionic nerve, and particularly that of the negative after-potential, was significantly depressed during the development of ACh depolarization as well as the slow negative potential, indicating that the 2 types of slow depolarization originated in the intraganglionic portion of the presynaptic fibers, presumably somewhere near or at the nerve terminals. ACh depolarization similar to that observed with bullfrog sympathetic ganglia was observed with rat superior cervical ganglia. The present experiments provide evidence that a certain part of the preganglionic nerve terminals is depolarized by the action of the transmitter released from their endings.