scholarly journals Loss of extrasynaptic acetylcholine sensitivity upon reinnervation of parasympathetic ganglion cells.

1979 ◽  
Vol 289 (1) ◽  
pp. 263-275 ◽  
Author(s):  
M J Dennis ◽  
P B Sargent
1945 ◽  
Vol 21 (1-2) ◽  
pp. 46-57
Author(s):  
N. AMBACHE ◽  
A. ST J. DIXON ◽  
E. A. WRIGHT

1. The effect of cooling on the properties of the crop and gizzard of the earthworm has been investigated. Evidence is advanced that the rhythmic movements of the ‘warm’ preparation are neurogenic in origin and peristaltic in nature. They are abolished by nicotine and by cooling, but not by atropine. 2. Acetylcholine contracts the muscle in the crop and gizzard. This effect is abolished by atropine. The excitability of the muscle to acetylcholine is not lost after cooling. 3. Peristalsis is accompanied in the ‘warm’ preparation by a continual liberation of acetylcholine. This is absent in cold preparations. The disappearance of rhythmic activity in these is associated with the loss of acetylcholine synthesis. 4. In the ‘warm’ crop and gizzard, potassium produces contraction which is enhanced by eserine, but not abolished by nicotine or by atropine. With higher doses of potassium, stimulation is followed by inhibition. After short periods of cooling, the motor response to potassium is lost, but the inhibitory effect is still present. Prolonged cooling abolishes both actions. It is suggested that the augmentor action of potassium is due to an intermediate release of acetylcholine from the cholinergic nerve endings, and the inhibitory action to a liberation of adrenaline from the adrenergic nerves in the crop and gizzard. 5. Calcium inhibits the rhythmic activity of ‘warm’ preparations, and the effect of potassium. It has no action on cooled preparations, and in these it does not affect the contractions produced by acetylcholine. It is suggested that calcium acts on ‘warm’ preparations by preventing the release of acetylcholine from cholinergic nerve endings. 6. The action of adrenaline on ‘warm’ preparations is twofold: small doses have an augmentor effect; larger doses are inhibitory. After cooling, adrenaline has no action by itself. It is suggested that the augmentor effect of adrenaline is due to an improvement in acetylcholine-transmission at the cholinergic nerve endings. 7. Small doses of barium contract the ‘warm’ preparation. This action is inhibited by calcium, abolished by nicotine, and is lost after cooling. It is suggested that the action of such doses of barium is due to a stimulation of parasympathetic ganglion cells. 8. The presence of multipolar nerve cells in the enteric plexus was demonstrated in histological sections of the crop and gizzard. These were found lying between the circular and longitudinal muscle layers, in a position analogous to that of Auerbach's plexus.


1987 ◽  
Vol 437 (1) ◽  
pp. 157-160 ◽  
Author(s):  
Robert A. Mitchell ◽  
Dorothy A. Herbert ◽  
David G. Baker ◽  
Carol B. Basbaum

1971 ◽  
Vol 177 (1049) ◽  
pp. 555-563 ◽  

1. The vagosympathetic trunks innervating the heart of the frog were cut on both sides. Two to 28 days following this denervation the chemosensitivity of the surface of the denervated neurons was explored with iontophoretic microapplication of ACh to restricted areas. 2. While in normally innervated neurons the synaptic areas alone are highly chemosensitive, after denervation the whole cell surface becomes sensitive to ACh. Synaptic transmission fails on the second day (30 to 40 h) after denervation (in frogs kept at 22 to 24 °C) and at the same time new chemoreceptive areas start to appear. After 4 to 8 days this development of chemosensitivity has reached a peak and remains at the same level for 4 weeks (the longest period of the present tests). 3. Measurements of chemosensitivity from different cells in different animals were compared. The finely localized chemosensitivity at synaptic areas in normally innervated neurons was of similar magnitude as the uniformly distributed sensitivity in denervated neurons.


PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0248106
Author(s):  
Ana Leonor Rivera ◽  
Bruno Estañol ◽  
Julio J. Macias-Gallardo ◽  
Guillermo Delgado-Garcia ◽  
Ruben Fossion ◽  
...  

Achalasia is a disease characterized by the inability to relax the esophageal sphincter due to a degeneration of the parasympathetic ganglion cells located in the wall of the thoracic esophagus. Achalasia has been associated with extraesophageal dysmotility, suggesting alterations of the autonomic nervous system (ANS) that extend beyond the esophagus. The purpose of the present contribution is to investigate whether achalasia may be interpreted as the esophageal manifestation of a more generalized disturbance of the ANS which includes alterations of heart rate and/or blood pressure. Therefore simultaneous non-invasive records of the heart inter-beat intervals (IBI) and beat-to-beat systolic blood pressure (SBP) of 14 patients (9 female, 5 male) with achalasia were compared with the records of 34 rigorously screened healthy control subjects (17 female, 17 male) in three different conditions: supine, standing up, and controlled breathing at 0.1 Hz, using a variety of measures in the time and spectral domains. Significant differences in heart rate variability (HRV) and blood pressure variability (BPV) were observed which seem to be due to cardiovagal damage to the heart, i.e., a failure of the ANS, as expected according to our hypothesis. This non-invasive methodology can be employed as an auxiliary clinical protocol to study etiology and evolution of achalasia, and other pathologies that damage ANS.


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