Abstract

Transmission blockade and depolarization evoked by nicotine are considered generally to be related and dependent events. In the present study, however, it was found that the characteristics of the blockade of transmission evoked by nicotine were not those usually associated with depolarization- induced ganglionic inexcitability. The following observations suggest that the blockade of transmission and the simultaneously occurring ganglionic depolarization were not causally related: 1) tetanic preganglionic stimulation antagonized the block occurring during depolarization evoked by nicotine; 2) tubocurarine antagonized depolarization evoked by nicotine, but enhanced the simultaneously occurring blockade of transmission; 3) the i.v. infusion of nicotine evoked a postganglionic discharge which was maintained when transmission was abolished; 4) discharges evoked by nonnicotinic ganglionic stimulating agents were enhanced during the blockade of transmission and depolarization evoked by nicotine. In many respects the blockade of transmission which coincided with depolarization was similar in character to the block which persisted beyond the period of depolarization evoked by nicotine. In addition, the data suggest that the site at which nicotine evokes ganglionic depolarization is distinct from that at which the compound blocks the actions of neurogenically released acetylcholine.