Acetylcholine Metabolism in Salivary Glands During the “Degeneration Secretion”

Abstract

The synthesis and breakdown of ACh have been studied in the submaxillary gland of the cat and in the parotid gland of the rabbit during the "degeneration secretion", that is during the first days after postganglionic parasympathetic denervation.The decrease in the cholinesterase activity found in both glands cannot be the cause of the secretory activity. It might, however, increase and prolong the secretion in the rabbit's parotid gland.The "degeneration secretion" and the disappearance of choline acetylase activity seem to occur simultaneously, thus showing that the secretory activity and the degeneration of the nerve endings probably are closely related to each other. The findings suLpport the hypothesis that the secretion is caused by an increased liberation of ACh from the degenerating nerve endings.A TRANSIENT secretory activity has been observed in the parotid gland of the cat after postganglionic parasympathetic denervation [Emmelin and Stromblad, 1958]. It appears during the first 3 days after section of the auriculotemporal nerve and occurs in periods of varying length alternating with periods of secretory inactivity. A similar phenomenon has also been found in the submaxillary and sublingual glands of the cat after partial postganglionic parasympathetic denervation [Emmelin, 1962]. The flow of saliva in these glands is not periodic but fairly regular while it occurs, that is between about 18 and 60 hr. after the denervation. It is enhanced by eserine and abolished by a small dose of atropine or local anaesthetics injected into the gland. This type of secretory activity in the salivary glands has been assumed to be due to an increase of a normal leakage of acetylcholine (ACh) from the postganglionic nerve endings during the degeneration period. It has therefore been called "degeneration secretion" [Emmelin, 1962]. This secretory activity is to be distinguished from the " paralytic secretion" [Burgen and Emmelin, 1961]. The "degeneration secretion" has also been observed more recently in the submaxillary and parotid glands of the rabbit [Ohlin, 1963].The present investigation deals with the ACh metabolism in the salivary glands during the time of the "degeneration secretion". The synthesis and breakdown of ACh is known to decrease after section of the postganglionic parasympathetic nerves [Stromblad, 1955;Nordenfelt, 1963] and an attempt has been made to correlate these changes in ACh metabolism with the secretory activity during "degeneration secretion".Choline acetylase and cholinesterase activities have been studied in the submaxillary gland of cats and the parotid gland of rabbits during the first days after postganglionic parasympathetic denervation. These two glands were chosen mostly for technical reasons. Both glands have a fairly high 103

Cholinesterase in the Submaxillary Gland of the Rat After Sympathetic Denervation

“…The finding that the ACh-synthesis of rat submaxillary glands increased after sympathetic ganglionectomy indicated that there was a growth of cholinergic neurones after this type of denervation [Nordenfelt, 1964 a]. In the present investigation it is shown that the ChE activities also increase significantly and that the rise is of about the same order as the ChAc increase after sympathetic denervation.…”

“…When investigations were made in other species it was not possible to demonstrate a change of the ChAc activity after postganglionic sympathetic denervation in salivary glands of the rabbit and dog, but in the submaxillary gland of the rat a ChAc increase was clearly shown [Nordenfelt, 1964 a], which was also verified by Ohlin and Perec [1967].…”

Degeneration secretion from parotid glands after section of the auriculotemporal nerves at different levels

“…The main cause, however, is that the leakage of acetylcholine from the post-ganglionic nerve endings which occurs normally but in quantities too small to evoke secretion (Emmelin, 1960(Emmelin, , 1965Assarson & Emmelin, 1964), temporarily increases above the secretory threshold. At one stage of degeneration the nerve endings can still synthesize acetylcholine (Nordenfelt, 1964) (Weiss & Hiscoe, 1948;Weiss, 1961Weiss, , 1963 has been supposed to be concerned with at least some of the components engaged in the transmission procedure at the endings, acetyleholinesterase and choline acetyltransferase (Feldberg & Vogt, 1948;Sawyer, 1946;Hebb & Waites, 1956;Lubinska, Niemierko & Oderfeld, 1961;Hebb & Silver, 1961;Lubinska, Niemierko & Zelena', 1963). It is also known that denervation supersensitivity, assumed to be due to loss of an action ofacetylcholine, appears earlier (Luco & Eyzaguirre, 1955;Emmelin & Malm, 1965) and that the ability to synthesize acetylcholine decreases earlier (Emmelin, Nordenfelt & Perec, 1966) the nearer the effector a cholinergic nerve has been cut.…”

Communications

“…Mott (1965) One or two days after post-ganglionic parasympathetic denervation saliva was found to flow from the parotid, submaxillary, and sublingual glands of anaesthetized cats. This 'degeneration secretion' was attributed to acetylcholine release from the nerve endings (Emmelin and Stromblad, 1958;Emmelin, 1962), which at a certain stage of degeneration still can synthesize acetylcholine but seem unable to retain it in a normal way (Nordenfelt, 1964). In the present experiments the early period of the 'degeneration secretion' was studied in parotid glands of cats.…”