An investigation of the nerve supply to thealt gland of the duck.

Abstract

Secretion can be produced from the salt gland of the duck by electrical stimulation of nerves reaching the gland and by the administration of parasympathomimetic drugs; the latency of this response is similar to that of the secretory response produced by intravenous salt loading and is similarly inhibited by atropine. The salt gland contains both acetyl‐ and butyrylcholinesterase; the former appears to be associated with nerve fibres which originate in cells occurring along the gland's secretory nerve and in its ganglion. There is no obvious difference in cholinesterase content of secreting and resting glands. Denervation of the salt gland, by an operation which includes removal of the ganglionic portion of the secretory nerve, abolishes secretory response to salt load and leads to disappearance of cholinesterase. Such denervated glands may be caused to secrete by administration of carbachol; this response is potentiated by concurrent salt loading. Section of the secretory nerve central to its ganglionic region, however, fails to abolish secretion in response to salt loading and does not alter cholinesterase content. Hexamethonium in large doses fails to influence the establishment or course of a secretory response to salt loading. These findings, coupled with the demonstration that cholinesterase staining in the secretory nerve is only seen in and distal to its ganglion cells, suggests that the cholinergic nerve supply to the gland is unusual. The findings support the concept that a cholinergic secretomotor mechanism can produce salt gland secretion. They also imply that any associated hormonal control of secretion cannot operate in the absence of intact peripheral nerve supply. The possibility is discussed that the ganglion cells of the secretory nerve may have an osmoreceptive function.