The Effect of Preganglionic Stimulation on the Acetylcholine and Choline Content of a Sympathetic Ganglion

Abstract

Preganglionic stimulation of the cat's superior cervical ganglion at 60/s for 2–8 min reduced the ganglion's acetylcholine (ACh) content by about 30%. With continued stimulation, the ACh stores gradually recovered within 15 min. However, when ganglia were allowed to rest following 4 min of stimulation at 60/s not only was there a rapid restoration of the ACh content, but the ACh levels rose to 130% of control after 10 min of rest. Under either of these experimental conditions the choline content increased transiently only after the ACh stores had returned to control values. The above data suggest that there may be a delay in the onset of maximal rates of ACh resynthesis induced by nerve stimulation and that ACh synthesis continues for several minutes after the cessation of the stimulus. In addition, the results are consistent with the concept that about one-third or more of the total ACh stores of a rested ganglion is in a form that can be readily mobilized for release. The observed rebound increase in the ACh content probably means that the ACh storage capacity is not normally saturable and that under most physiological conditions the ACh levels are maintained within certain limits by a precise control of ACh synthesis.

Regulation by patterned preganglionic neural activity of transmitter stores in a sympathetic ganglion.

“…This conclusion was confirmed in a further series of experiments in which the frequency within the 0 5 s trains was raised to 40/s. As expected from the earlier work of Friesen & Khatter (1971) and Birks & Fitch (1974), when the 40/s stimulation was delivered continuously for 60 min and the ganglia removed without rest, the ACh stores were not increased, indeed it appeared that they might in fact be lower than the stores of the control ganglia. As shown in Table 3, the ratio in four experiments was 96 + 11 %.…”

“…One way in which these different effects of nerve activity might increase ACh synthesis over the demand of release to increase ACh stores is by promoting entry of choline into the nerve terminals. There is evidence that the intracellular concentration of choline rises during high-frequency stimulation (Friesen & Khatter, 1971). Choline transport is sodium-dependent, linked to activity of the sodium pump (Yamamura & Snyder, 1973) and would be expected to be sensitive to the transmembrane electrochemical gradient.…”

“…The mean frequency of patterned stimulation at which the increase in stores takes place during activation is well within the physiological range of sympathetic discharging, which has variously been reported as 2-3/s in anaesthetized animals (Polosa, 1968;Skok, 1973). The report by Bourdois, McCandless & MacIntosh (1975) of a 30 % increase in stores of ganglia stimulated for 60 min at 50/s and removed without rest may represent some ability of ganglia to accumulate ACh during unphysiological levels of activity, but see Birks & MacIntosh (1961), Friesen & Khatter (1971), Birks & Fitch (1974) as well as the observation above that the stores were not increased in ganglia stimulated at 40/s when they were removed without rest. Indeed because ganglia do not follow faithfully excitation at frequencies above 40/8 (see below) it might be considered that the increases observed by Bourdois et al (1975) with 50/s stimulation resulted from intermittent impulse conduction in preganglionic fibres unable to carry continuous high frequency bombardment.…”

Enteric GABA‐containing nerves projecting to the guinea‐pig inferior mesenteric ganglion modulate acetylcholine release.

“…The preparations were superfused with Krebs-Ringer buffer containing 0 01 % collagenase (Type 1A, Sigma Chemical Co., St Louis, MO, USA) for 10 min followed by a 20 min rinse with Krebs-Ringer buffer alone (Stapelfeldt & Szurszewski, 1989) to facilitate diffusion of released [3H]acetylcholine out of the ganglion and into the superfusate. It was shown in a previous study that similar treatment of the inferior mesenteric ganglion did not affect fast or slow synaptic transmission (Stapelfeldt & Szurszewski, 1989 (Friesen & Khatter, 1971). After loading, the preparations were washed for 30 min with Krebs-Ringer buffer containing 50 /M physostigmine and 10/M hemicholinium-3 (Sigma Chemical Co.) (control solution).…”

Synthesis of Acetylcholine from Acetate in a Sympathetic Ganglion

“…It is now clear that there is an increase in ganglionic ACh content during a resting period following a period of intense preganglionic stimulation (Rosenblueth et al, 1939;Friesen and Khatter, 1971;Birks and Fitch, 1974;Bourdois et al, 1975;Birks, 1977;O'Regan and Collier, 1981). This implies that there is an increase in ACh synthesis in this poststimulation period in the absence of preganglionic stimulation.…”