Sympathetic nerves, salivary secretion, and the parched mouth of fear: unraveling historical perspectives on persistent contradiction in physiology textbooks.

Abstract

We have observed two starkly contradictory notions regarding the sympathetic influence on the salivary outflow in discussions with our students. Most of them believe that sympathetic nerves decrease salivation and are antagonistic to parasympathetic nerves. Some students, however, show awareness of the cooperative stimulatory action of both types of autonomic fibers. We have found a similar dichotomy in the descriptions of the sympathetic effect on secretion of the main salivary glands and their inconsistent illustrations in Anatomy/Physiology textbooks. We have investigated the historical roots of this discrepancy. Ludwig discovered excitatory actions of both parasympathetic and sympathetic nerves on salivary flow by 1856. The next year, Czermak proposed the hypothesis of an inhibitory effect of sympathetic nerves, observing their interference with salivation induced by the chorda tympani (i.e., parasympathetic) stimulation. Bernard and Eckhard soon confirmed Ludwig's findings, but Czermak's notion persisted because sympathetically evoked salivation was unstable and potentially abatable by glandular vasoconstriction. The salivary secretory response to moderate sympathetic nerve electrostimulation was reaffirmed by Langley who also discovered salivation in response to adrenaline injection at the beginning of the 20th century. A few years later, Cannon, on a purely theoretical basis, attributed the sensation of dry mouth occasionally associated with fear to hyposalivation induced by elevated sympathetic discharge. Despite subsequent researchers' inability to find unequivocal evidence of salivary flow reduction by sympathetic activation, Cannon's assumption gained acceptance in some textbooks. Most Anatomy/Physiology textbook authors, however, recognized the excitatory action of sympathetic nerves on salivary glands established by Ludwig and Bernard.