Acetylcholine synthesis and its dependence on nervous activity

Abstract

The findings discussed in this paper mainly derived from studies on salivary glands, serving as model organs, indicate that the capacity to form the neurotransmitter acetylcholine, as judged by the activity of choline acetyltransferase, is influenced by the traffic of nerve impulses, as a long term effect. In the glands, choline acetyltransferase seems to be exclusively localized to the cholinergic nerves. In the postganglionic parasympathetic nerves of the glands, the activity of choline acetyltransferase decreases when the flow of secretory impulses in these nerves is abolished or reduced either by isolating the nerves from the central nervous system, surgically or pharmacologically, or by diminishing the reflex activation of the glands from the mouth. The opposite occurs when the reflex activation of the salivary glands is enhanced, i.e. the activity of choline acetyltransferase increases. Observations on various other organs are quoted in support of the view that the traffic of nerve impulses is of importance for the activity of the enzyme. An increase in choline acetyltransferase activity also occurs in some salivary glands after sympathetic denervation. This puzzling observation is discussed in relation to impulse traffic. Increased nerve impulse traffic and collateral sprouting seem to be responsible for the rapid restitution of choline acetyltransferase activity from a low level in an organ partially deprived of its cholinergic nerve supply.

Effects of duct ligation on choline acetyltransferase activity in salivary glands of rats

“…Such a possibility has also been considered by the radiochemical assay of choline acetyltransferase in the heart (White & Wu 1973) and placenta (Welsch 1977). Using the control incubations described above, the choline acetyltransferase activity was found to be very low in denervated parotid glands, a finding which agrees with previous observations (see Ekstrom 1978). The remaining enzyme activity, about 1 % of that of the contralateral gland, can be accounted for, since some nerves persist in the gland after the denervation procedure ( A h & Ekstrom 1976).…”

“…In a previous study (Ekstrom 1975) where the ducts of several major salivary glands were tied in an animal, the intact gland(s) gained in weight and showed increased choline acetyltransferase activity compared with control glands in unoperated animals; this was thought to reflect increased traffic of secretory impulses in the nervous pathways to the gland (see Ekstrom 1978). In a previous study (Ekstrom 1975) where the ducts of several major salivary glands were tied in an animal, the intact gland(s) gained in weight and showed increased choline acetyltransferase activity compared with control glands in unoperated animals; this was thought to reflect increased traffic of secretory impulses in the nervous pathways to the gland (see Ekstrom 1978).…”

“…The secretory capacity of such a gland is greatly reduced both in response to secretagogue drugs (Ohlin & Perec 1967, Emmelin, Garrett & Ohlin 1974 and to nerve stimulation (Emmelin et al 1974). Choline acetyltransferase, the acetylcholine synthesizing enzyme, is confined to the cholinergic nerves in salivary glands (see Ekstrom 1978), and in the present study the effect of duct ligation on this enzyme was investigated in the parotid and submaxillary glands of rats. The activity of choline acetyltransferase was estimated by a radiochemical method; however, difficulties were encountered in identifying acetylcholine and these were solved by using additional controls in the assay procedure.…”

“…gland may have caused decreased enzyme activity (seeEkstrom 1978). Afferent nerve impulses have been shown t o arise from salivary glands (Kawamura & Funakoshi 1964; see also…”

Glucocorticoid-induced hypertension in rats: role of the central muscarinic cholinergic system

“…Ekstrom (1978) suggested that changes of CHAT activity were produced by con¬ comitant alterations in cholinergic nerve activity. In view of this we explored the sodium-dependent, HC-3-inhibitable, high-affinity choline uptake.…”