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

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.

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%.


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.


1970 ◽  
Vol 118 (5) ◽  
pp. 813-818 ◽  
Author(s):  
P. Banks

1. Superior cervical ganglia from the guinea pig carry out an energy-dependent incorporation of l-[14C]valine into protein in vitro. 2. Stimulation of the preganglionic nerve at a physiological frequency for more than a few minutes decreases the ability of the ganglia to incorporate labelled valine into protein.


1993 ◽  
Vol 113 (2) ◽  
pp. 146-151 ◽  
Author(s):  
Tian-Ying Ren ◽  
E. Laurikainen ◽  
W. S. Quirk ◽  
J. M. Miller ◽  
A. L. Nuttall

2003 ◽  
Vol 94 (1) ◽  
pp. 220-226 ◽  
Author(s):  
Weirong Zhang ◽  
Paul W. Davenport

It has been demonstrated that phrenic nerve afferents project to somatosensory cortex, yet the sensory pathways are still poorly understood. This study investigated the neural responses in the thalamic ventroposteriolateral (VPL) nucleus after phrenic afferent stimulation in cats and rats. Activation of VPL neurons was observed after electrical stimulation of the contralateral phrenic nerve. Direct mechanical stimulation of the diaphragm also elicited increased activity in the same VPL neurons that were activated by electrical stimulation of the phrenic nerve. Some VPL neurons responded to both phrenic afferent stimulation and shoulder probing. In rats, VPL neurons activated by inspiratory occlusion also responded to stimulation on phrenic afferents. These results demonstrate that phrenic afferents can reach the VPL thalamus under physiological conditions and support the hypothesis that the thalamic VPL nucleus functions as a relay for the conduction of proprioceptive information from the diaphragm to the contralateral somatosensory cortex.


2007 ◽  
Vol 98 (3) ◽  
pp. 1102-1107 ◽  
Author(s):  
Serajul I. Khan ◽  
John A. Burne

Muscle cramp was induced in one head of the gastrocnemius muscle (GA) in eight of thirteen subjects using maximum voluntary contraction when the muscle was in the shortened position. Cramp in GA was painful, involuntary, and localized. Induction of cramp was indicated by the presence of electromyographic (EMG) activity in one head of GA while the other head remained silent. In all cramping subjects, reflex inhibition of cramp electrical activity was observed following Achilles tendon electrical stimulation and they all reported subjective relief of cramp. Thus muscle cramp can be inhibited by stimulation of tendon afferents in the cramped muscle. When the inhibition of cramp-generated EMG and voluntary EMG was compared at similar mean EMG levels, the area and timing of the two phases of inhibition (I1, I2) did not differ significantly. This strongly suggests that the same reflex pathway was the source of the inhibition in both cases. Thus the cramp-generated EMG is also likely to be driven by spinal synaptic input to the motorneurons. We have found that the muscle conditions that appear necessary to facilitate cramp, a near to maximal contraction of the shortened muscle, are also the conditions that render the inhibition generated by tendon afferents ineffective. When the strength of tendon inhibition in cramping subjects was compared with that in subjects that failed to cramp, it was found to be significantly weaker under the same experimental conditions. It is likely that reduced inhibitory feedback from tendon afferents has an important role in generating cramp.


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