A Prolonged After-Effect of Intense Synaptic Activity on Acetylcholine in a Sympathetic Ganglion

1975 ◽  
Vol 53 (1) ◽  
pp. 155-165 ◽  
Author(s):  
P. S. Bourdois ◽  
D. L. McCandless ◽  
F. C. MacIntosh

The finding was confirmed that there is a "rebound" increase of stored acetylcholine (ACh) in cat superior cervical ganglia conditioned by prolonged preganglionic stimulation at a frequency high enough to cause initial depletion of the store. Ganglia removed immediately after 60 min of continuous or interrupted stimulation at 50 Hz, with chloralose as anesthetic, contained about 30% more ACh than their unconditioned controls; the rebound rose to about 60% after 15 min of rest and then subsided with an apparent half-time of about 2 h. Tests with hemicholinium, combined with hexamethonium or tubocurarine, showed that rebound ACh was located pre-synaptically and could be released by nerve impulses; but conditioned ganglia perfused with an eserine-containing medium did not release more ACh than their unconditioned controls, except in circumstances in which the mobilization of ACh from a reserve store appeared to be the rate-limiting process for release. The appearance of rebound ACh during and after conditioning stimulation was suppressed by hexamethonium and by tubocurarine, neither of which has much effect on ACh turnover in ganglia excited at lower frequencies, but not by atropine, noradrenaline, or phenoxybenzamine. The formation of rebound ACh is thus contingent on the postsynaptic nicotinic response to released ACh, and may represent an augmentation of the transmitter store in structures remote from the release sites.

1969 ◽  
Vol 47 (2) ◽  
pp. 127-135 ◽  
Author(s):  
B. Collier ◽  
F. C. MacIntosh

Choline (Ch) and acetylcholine (ACh) uptake and release were measured by a combination of tracer and bioassay techniques in perfused superior cervical ganglia of the cat during rest and repetitive preganglionic stimulation. The uptake of labelled ACh as such was small; but when Ch (methyl-3H labelled) was present at physiological concentration (1.5 μg/ml) in the perfusion fluid, its incorporation into the ACh and free Ch pools of the ganglion proceeded linearly in the absence of stimulation, was accelerated by stimulation, and was inhibited by hemicholinium but not by hexamethonium. Up to 85% of ganglionic ACh could be replaced by labelled ACh during a 1-h stimulation period. On subsequent perfusion with fluid containing unlabelled Ch, labelled Ch was lost but labelled ACh was retained and could be released by stimulation, either as ACh in the presence or as Ch in the absence of eserine. The output of label during stimulation was approximately doubled by eserine but was unaffected by hemicholinium, which, however, prevented the formation and release of newly synthesized ACh. It appears that about half the Ch formed from released ACh is immediately recaptured and resynthesized into ACh. Newly synthesized ACh rapidly gains access to the releasable transmitter pool and may be preferentially released.


1971 ◽  
Vol 49 (5) ◽  
pp. 375-381 ◽  
Author(s):  
A. J. D. Friesen ◽  
J. C. Khatter

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.


Author(s):  
J. Quatacker ◽  
W. De Potter

Mucopolysaccharides have been demonstrated biochemically in catecholamine-containing subcellular particles in different rat, cat and ox tissues. As catecholamine-containing granules seem to arise from the Golgi apparatus and some also from the axoplasmic reticulum we examined wether carbohydrate macromolecules could be detected in the small and large dense core vesicles and in structures related to them. To this purpose superior cervical ganglia and irises from rabbit and cat and coeliac ganglia and their axons from dog were subjected to the chromaffin reaction to show the distribution of catecholamine-containing granules. Some material was also embedded in glycolmethacrylate (GMA) and stained with phosphotungstic acid (PTA) at low pH for the detection of carbohydrate macromolecules.The chromaffin reaction in the perikarya reveals mainly large dense core vesicles, but in the axon hillock, the axons and the terminals, the small dense core vesicles are more prominent. In the axons the small granules are sometimes seen inside a reticular network (fig. 1).


1975 ◽  
Vol 53 (3) ◽  
pp. 451-457 ◽  
Author(s):  
J. C. Khatter ◽  
A. J. D. Friesen

Preganglionic stimulation of the cat's superior cervical ganglion in the presence of hemicholinium-3 (HC-3) produced the expected depletion of acetylcholine (ACh) stores, but failed to cause a corresponding reduction in the choline content. These results suggest that either HC-3 possesses an intracellular site of action or that in lower doses it selectively inhibits a specialized choline transport system in cholinergic nerves. At a dose of 2 mg/kg, HC-3 probably blocked ACh synthesis completely in ganglia stimulated at 20 Hz. Under these conditions, there was a rapid depletion of ACh to about 50% of control levels during the first 5 min of stimulation and thereafter the rate of decline in ACh levels proceeded at a much slower pace. Since the 2 mg/kg dose of HC-3 did not raise plasma choline concentrations, it may be assumed that non-specialized choline transport systems in other tissues were not significantly inhibited by this dose of HC-3. However, when the dose of HC-3 was increased to 4 mg/kg, plasma choline levels increased by 58%.


1969 ◽  
Vol 47 (2) ◽  
pp. 119-126 ◽  
Author(s):  
B. Collier ◽  
Celia Lang

Cat's superior cervical ganglia were perfused with Locke's solution containing choline (Ch) at physiological concentration but labelled (methyl-3H), and the radioactive products in extracts of such ganglia were identified by a combination of selective precipitation and chromatographic tests. Ch was incorporated into acetylcholine (ACh), into phosphorylcholine (PCh), and into phospholipid. The rate of formation of PCh and phospholipid from Ch was measured to be about 2 ng/min of each, and this rate was unaffected by activity or by hemicholinium. Free Ch liberated by PCh or phospholipid turnover is unlikely to be an important source of Ch for ACh synthesis under physiological conditions.


1963 ◽  
Vol 41 (1) ◽  
pp. 2627-2636 ◽  
Author(s):  
Mervyn C. L. Weir ◽  
H. McLennan

Injection of the catecholamines, and particularly adrenaline, has been found always to depress synaptic transmission in a sympathetic ganglion. Although an adrenaline-like substance is released upon preganglionic stimulation, this is not believed to have any physiological significance.


1981 ◽  
Vol 240 (1) ◽  
pp. R38-R43 ◽  
Author(s):  
C. Gonzalez ◽  
Y. Kwok ◽  
J. Gibb ◽  
S. Fidone

The carotid bodies, along with the superior cervical ganglia and the adrenal glands, were removed from rabbits and cats and the activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine biosynthesis, was assayed by the method of Nagatsu (Anal. Biochem. 9: 122-126, 1964). The activities of the enzyme, in nmols tyrosine hydroxylated x h-1 x mg tissue-1, were: carotid body, rabbit 1.29, cat 0.84; superior cervical ganglion, rabbit 8.66, cat 4.97; adrenal gland, rabbit 0.95, cat 2.25. With respect to the carotid body, each of the following experimental procedures resulted in a long-term increase in TH activity in the rabbit but not in the cat: 1) severe hypoxia (5% O2 in N2 for 1 h, assay of TH 48 h later); 2) chronic transection of the carotid sinus nerve (assay of TH at 12-15 days); or 3) administration of reserpine (10 mg/kg at 0 and 24 h, assay of TH at 48 h). These observations are compared with our previous findings for rat carotid body and are discussed in relation to the role of catecholamines in chemoreception, and, in particular, to the reported differences in dopamine action in the carotid bodies of these different species. Our results also suggest species differences with respect to the participation of the sympathoadrenal system in response to reserpine and hypoxic stress.


1999 ◽  
Vol 80 (5) ◽  
pp. 326-331
Author(s):  
I. N. Volkova ◽  
E. M. Volkov ◽  
R. A. Giniatullin ◽  
A. L. Zefirov ◽  
G. I. Poletaev ◽  
...  

The works of A.V. Kibyakov, devoted to the physiology of mediators, and above all his discovery of the participation of chemicals in the transmission of nerve impulses in the sympathetic ganglion of a cat, served as one of the cornerstones in the foundation of modern neurophysiology. Research A.V. Kibyakov for many decades determined the scientific interests of his immediate students and followers.


1963 ◽  
Vol 18 (2) ◽  
pp. 317-324 ◽  
Author(s):  
Margot R. Craw ◽  
H. P. Constantine ◽  
J. A. Morello ◽  
R. E. Forster

We have measured the rate at which the O2 tension rises in a partially oxygenated suspension of normal human red cells at 37 C as a result of a sudden rise in CO2 tension (the Bohr shift) in a Hartridge-Roughton rapid reaction apparatus. A Teflon covered platinum electrode was used to measure O2 tension. The rise in O2 tension had an average half time of 0.12 sec following increments of 18–65 mm Hg in CO2 tension in twelve experiments on the blood of three normal individuals. The comparable movement of O2 out of the red cell as a result of a decrease in ambient O2 tension at a constant CO2 tension had an average half time of 0.012 sec in four experiments on the blood from the same three subjects. This suggests that the velocities of the reactions of CO2 are rate-limiting in the Bohr shift. Acetazolamide (10-3 m) slowed the rate of the Bohr shift to less than one-seventh; no measurable change in O2 tension occurred until about 0.03 sec. measurable change in O2 tension occurred until about 0.03 sec. Submitted on July 2, 1962


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