An attempt to localize the site of action of different agents within cholinergic motor neurones of the myenteric plexus-longitudinal muscle preparation of the guinea pig ileum by the triple bath method

1991 ◽  
Vol 30 (5) ◽  
pp. 517-525 ◽  
Author(s):  
O. Kadlec ◽  
I. Šeferna ◽  
J. Ševčík
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Longitudinal Muscle ◽  
Muscle Preparation ◽  
Guinea Pig Ileum ◽  
Site Of Action ◽  
Motor Neurones

Opiatelike actions of eseroline, an eserine derivative

1981 ◽  
Vol 59 (3) ◽  
pp. 307-310 ◽  
Author(s):  
K. Jhamandas ◽  
J. Elliott ◽  
M. Sutak
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Vas Deferens ◽  
Longitudinal Muscle ◽  
Rat Vas Deferens ◽  
Anticholinesterase Activity ◽  
Muscle Preparation ◽  
Guinea Pig Ileum ◽  
Anesthetized Rats ◽  
Release Of Acetylcholine

Eseroline, an eserine derivative without anticholinesterase activity, was tested in several systems for opiatelike activity. Eseroline depressed the twitch of the field-stimulated guinea pig ileum myenteric plexus longitudinal muscle preparation but failed to depress the twitch of the rat vas deferens. Intraperitoneal injections of eseroline in rats induced naloxone-antagonizable analgesia and catalepsy. Eseroline failed to influence the release of acetylcholine from the cortex of anesthetized rats. These observations have implications for studies in which eserine is used as a pharmacological tool.

Endogenous Acetylcholine Release and Labelled Acetylcholine Formation from [3H]Choline in the Myenteric Plexus of the Guinea-Pig Ileum

1975 ◽  
Vol 53 (4) ◽  
pp. 566-574 ◽  
Author(s):  
John C. Szerb
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Longitudinal Muscle ◽  
Muscle Preparation ◽  
Guinea Pig Ileum ◽  
Low Concentrations ◽  
Constant Rate ◽  
Release Of Acetylcholine ◽  
Small Pool

The spontaneous release of acetylcholine (ACh) from the guinea-pig myenteric plexus – longitudinal muscle preparation superfused at a constant rate in the presence of physostigmine was 10 nmol∙g−1∙h−1. This release was decreased to one-third by tetrodotoxin or by MnCl2 and increased 2.5 times by 0.1 Hz and 20 times by 16 Hz stimulation. The formation of [3H] ACh from [3H]choline increased from 3 to 33 nmol∙g−1∙h−1 when the concentration of [3H]choline was increased from 1 μM to 50 μM. The rate of [3H] ACh formation was not affected by tetrodotoxin, MnCl2, or physostigmine in the absence of stimulation. It was increased by 50% by 0.1 Hz and by 100% by 16 Hz stimulation during the first 9 min of exposure to [3H]choline but not subsequently. The myenteric plexus – longitudinal muscle preparation contains 200 nmol/g choline. Results suggest that the apparent small [3H]ACh formation from low concentrations of [3H]choline is due to the dilution of [3H]choline by endogenous choline. The major part of [3H]ACh formation appears to be due to the intracellular turnover of ACh while the evoked release of [3H]ACh appears to originate from a small pool.

Somatostatin modulation of peptide-induced acetylcholine release in guinea pig ileum

1984 ◽  
Vol 246 (5) ◽  
pp. G509-G514 ◽  
Author(s):  
D. H. Teitelbaum ◽  
T. M. O'Dorisio ◽  
W. E. Perkins ◽  
T. S. Gaginella
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Longitudinal Muscle ◽  
Guinea Pig Ileum ◽  
Gut Motility ◽  
Release Of Acetylcholine

The peptides caerulein, neurotensin, somatostatin, and substance P modulate the activity of intestinal neurons and alter gut motility. We examined the effects of these peptides on acetylcholine release from the myenteric plexus and intestinal contractility in vitro. Caerulein (1 X 10(-9) M), neurotensin (1.5 X 10(-6) M), and substance P (1 X 10(-7) M) significantly enhanced the release of [3H]acetylcholine from the myenteric plexus of the guinea pig ileum. This effect was inhibited by tetrodotoxin (1.6 X 10(-6) M). Somatostatin (10(-6) M) inhibited caerulein- and neurotensin-evoked release of acetylcholine but did not inhibit release induced by substance P. Caerulein, neurotensin, and substance P caused contraction of the guinea pig ileal longitudinal muscle. Somatostatin inhibited the contractions induced by caerulein and neurotensin. In contrast, substance P-induced contraction was not inhibited significantly by somatostatin. Thus, in the guinea pig ileum, caerulein-, neurotensin-, and substance P-induced contractility is due, at least in part, to acetylcholine release from the myenteric plexus. The ability of somatostatin to inhibit peptide-induced contractility is selective, and its mechanism may be attributed to inhibition of acetylcholine release.

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