scholarly journals Muscarinic presynaptic inhibition of synaptic transmission in myenteric plexus of guinea-pig ileum.

1982 ◽  
Vol 333 (1) ◽  
pp. 141-149 ◽  
Author(s):  
K Morita ◽  
R A North ◽  
T Tokimasa
Keyword(s):  
Guinea Pig ◽  
Synaptic Transmission ◽  
Myenteric Plexus ◽  
Presynaptic Inhibition ◽  
Guinea Pig Ileum

Interaction of dynorphin with neurotensin on the guinea pig ileum myenteric plexus

Life Sciences ◽  
1982 ◽  
Vol 31 (16-17) ◽  
pp. 1825-1828 ◽  
Author(s):  
Yuang-Xiang Zhu ◽  
J.Pablo Huidobro-Toro ◽  
Nancy M. Lee ◽  
Horace H. Loh ◽  
E.Leong Way
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Guinea Pig Ileum

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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