The origin of acetylcholine released from guinea‐pig intestine and longitudinal muscle strips

Abstract

SUMMMARY1. Strips of longitudinal muscle can be obtained from guinea-pig ileum either retaining or free from Auerbach's plexus.2. The denervated strip is unresponsive to electrical stimulation by brief shocks, whether given singly or in trains; it also fails to respond to nicotine or dimethylphenylpiperazinium iodide (DMPP), and eserine causes no spasm.3. Denervated strips neither contain detectable acetylcholine ( < 0 4 ng/ mg), nor release it spont&neously (< 5 pg/mg/min) or in response to stimulation (< 31 pg/mg/min). The acetylcholine metabolism of the innervated strip is therefore that of the adherent Auerbach's plexus. Innervated strips had a mean acetylcholine content of 28 ng/mg, a mean resting output of 94 pg/mg/min and an output in response to stimulation at 10 c/s of 700-1200 pg/mg/min.4. By comparing the responses of innervated and denervated strips it was concluded that arecoline, methylfurmethide, a,8l-ethylal-y-trimethylammonium propanediol iodide (2268 F), muscarine, histamine, tremorine, oxytocin, and substance P, like acetylcholine, act primarily on the smooth muscle directly; and that angiotensin, barium, potassium, m-bromophenyl choline ether and 5-hydroxytryptamine have a progressively increasing proportionate effect on the nerve plexus. Nicotine and DMPP were inactive in the absence of the plexus.5. The longitudinal muscle with its accompanying plexus contains about one quarter of the acetylcholine of the whole ileum, and is responsible for about one fifth of the output to electrical stimulation.6. The volley output of acetylcholine by the innervated strip declines sharply as rate of stimulation increases. Output of acetylcholine was reduced by morphine and by cocaine, particularly when resting or when stimulated at low rates.

Novel pharmacological profile of muscarinic receptors mediating contraction of the guinea-pig uterus

“…Guinea-pigs (Pirbright-white, 300-400 g) of either sex were killed by cervical dislocation. Left atria and ileallongitudinal muscle strips (Paton and Zar 1968) were set up in 6 ml organ baths, under 500 mg tension, in oxygenated (95% 0 2 + 5% C0 2 ) Tyrode solution (32°C) composed of (mmol/ 1): NaCI 137.0, KCI 2.7, CaC1 2 1.8, MgC1 2 1.05, NaHC0 3 11.9, NaH 2 P0 4 0.42 and ( + )-glucose 5.6. Arecaidine propargyl ester (Moseret al 1989) was used as an agonist.…”

Affinity profiles of hexahydro-sila-difenidol analogues at muscarinic receptor subtypes

“…A force-displacement transducer connected to a Heilige amplifier and a multichannel recorder were used for these measurements. Strips of ileal longitudinal muscle (1.5 cm length) were prepared according to Paton and Zar (1968). The tissue responses to the cumulative addition of arecaidine propargyl ester were measured as isotonic contractions and recorded as wi th the atria.…”

Action of morphine on the neuro‐effector transmission in the guinea‐pig ileum and in the mouse vas deferens.

“…About 10 cm of the terminal ileum was discarded, and the lumen of the ileum was flushed with Krebs solution. The longitudinal cut strip together with the myenteric plexus (about 25mm in length and 1-5-2-0 mm in width) and the circularly cut strip together with the myenteric plexus (10-12 mm in length and 1-5-2-0 mm in width) were prepared for use in the micro-electrode and double sucrose gap methods, according to the procedures described by Paton & Zar (1968). In some experiments, the ileum was incised along the mesentery, and the mucosal layer was carefully removed.…”

“…ITO AND K. TAJIMA DISCUSSION Morphine hyperpolarizes the membrane of the neurone soma in the Auerbach's plexus in the guinea-pig ileum (North & Tonini, 1977). The suppression of firing of myenteric neurones induced by the hyperpolarization in the presence of morphine might explain the reduction in the resting output of acetylcholine from the longitudinal preparations of guinea-pig ileum observed by Paton (1957), Paton & Zar (1968).…”

“…1975). There is evidence that suppression of the evoked acetylcholine release by morphine is a direct action on the cholinergic neurones which innervate the longitudinal muscle (Paton & Zar, 1968;Waterfield & Kosterlitz, 1974). Dingledine & Goldstein (1976) demonstrated that the ability of field stimulation to induce contractions and of morphine to inhibit these contractions was vitually unchanged when the two known excitatory inputs to the cholinergic motor neurones in the Auerbach's plexus in the ileum were eliminated by receptor blockade.…”