Blockade by tetanus and botulinum A toxin of postganglionic cholinergic nerve endings in the myenteric plexus

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.

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Relationship between acetylcholine content and release in the cat's cerebral cortex

Canadian Journal of Physiology and Pharmacology ◽

10.1139/y70-113 ◽

1970 ◽

Vol 48 (11) ◽

pp. 780-790 ◽

Cited By ~ 80

Author(s):

J. C. Szerb ◽

H. Malik ◽

E. G. Hunter

Keyword(s):

Cerebral Cortex ◽

Negative Correlation ◽

Significant Negative Correlation ◽

Nerve Endings ◽

Cholinesterase Inhibition ◽

Electrolytic Lesion ◽

Ach Release ◽

Cholinergic Nerve ◽

The Brain ◽

High Output

Cortical acetylcholine (ACh) release and content were measured in non-anesthetized pretrigeminally sectioned or in Dial-anesthetized cats. In 28 pretrigerninally sectioned cats a very highly significant negative correlation between ACh content and output was found. In the same preparations, 15 mg/kg pentobarbital or electrolytic lesion in the rostral midbrain decreased ACh output and increased content. Atropine (1 mg/kg i.v. or 1 μg/ml topically) increased ACh output fourfold without significantly altering content. A larger dose of atropine (25 mg/kg i.v.) increased output ninefold and decreased ACh content. In Dial-anesthetized preparations, picrotoxin-induced ACh release was accompanied by a decrease in ACh content. Pretreatment with atropine in the same preparation resulted in an enhanced effect of picrotoxin on both output and content while atropine alone (1 mg/kg i.v.) raised ACh output without decreasing content. In pretrigerminally sectioned non-anesthetized preparations, hemicholinium-3 (HC-3) did not reduce ACh output significantly but reduced content. In the presence of atropine, HC-3 rapidly reduced the high output and decreased ACh content faster than without atropine. Cortical ACh content determined following cholinesterase inhibition (surplus ACh) did not follow changes in ACh output. It is concluded that cortical cholinergic nerve endings do not maintain constant ACh content at various output rates in contrast to peripheral cholinergic nerve endings. Atropine enhances ACh output probably both by increasing ACh synthesis and by blocking an inhibitory loop. The amount of ACh released per minute varies from 1/500 to 1/13 of the amount present depending on the activity of cholinergic fibers. ACh collected from the surface of the brain does not originate directly from surplus ACh.

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