Answers are grounded in this paper and cite their sources.
In cats under chloralose anaesthesia micro-electrodes were inserted into parotid gland cells. 2. The average resting potential was found to be -35 . 6 +/- 4 . 7 (S.D.) mV. 3. Stimulation of the auriculo-temporal nerve caused hyperpolarizing, or occasionally depolarizing, secretory potentials of 5--10 mV, which were abolishable with atropine. 4. Stimulation of the cervical sympathetic trunk regularly caused, after long latency (several seconds), slow depolarizations of 15--20 mV, accompanied by a decrease in input resistance. They were antagonized by practolol and therefore assumed to be mediated by beta 1-adrenoceptors. Occasionally hyperpolarization, ascribed to an effect on alpha-adrenoceptors, was observed. 5. In many units the slow depolarization on sympathetic stimulation was preceded by short-lasting hyperpolarizing (sometimes depolarizing) transients. They resembled the evoked cholinergic responses but could be abolished not only by atropine but also by guanethidine.
No takes yet. Share an insight, caveat, or question.
Emmelin et al. (1980) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: