Calcitonin gene-related peptide: A potent new peptidergic messenger substance in the myenteric plexus of guinea-pig small intestine

1986 ◽  
Vol 91 (4) ◽  
pp. 1062
Author(s):  
J.M. Palmer ◽  
M. Schemann ◽  
K. Tamura ◽  
J.D. Wood
Keyword(s):  
Small Intestine ◽  
Guinea Pig ◽  
Myenteric Plexus ◽  
Calcitonin Gene Related Peptide ◽  
Related Peptide ◽  
Calcitonin Gene

scholarly journals Effects of capsaicin and 5-HT3 antagonists on 5-hydroxytryptamine-evoked release of calcitonin gene-related peptide in the guinea-pig heart

1993 ◽  
Vol 108 (2) ◽  
pp. 431-435 ◽  
Author(s):  
Manuela Tramontana ◽  
Sandro Giuliani ◽  
Elena Bianco ◽  
Alessandro Lecci ◽  
Carlo A. Maggi ◽  
...  
Keyword(s):  
Guinea Pig ◽  
Calcitonin Gene Related Peptide ◽  
Guinea Pig Heart ◽  
Related Peptide ◽  
Calcitonin Gene

Stimulation of acetylcholine release in myenteric plexus by calcitonin gene-related peptide

1990 ◽  
Vol 259 (6) ◽  
pp. G934-G939 ◽  
Author(s):  
M. W. Mulholland ◽  
S. Jaffer
Keyword(s):  
Myenteric Plexus ◽  
Acetylcholine Release ◽  
Calcitonin Gene Related Peptide ◽  
Ach Release ◽  
Related Peptide ◽  
Calcitonin Gene ◽  
Dose Dependent Increase ◽  
Dose Dependent ◽  
Dependent Mechanism ◽  
Stimulation Of

The effects of calcitonin gene-related peptide (CGRP) on acetylcholine (ACh) release from myenteric plexus neurons in primary culture were investigated. CGRP (10(-12) to 10(-6) M) produced a dose-dependent increase in [3H]ACh release. The ACh release caused by CGRP was significantly inhibited (74 +/- 24%) by preincubation with dideoxyadenosine but was increased more than threefold by preincubation with theophylline. Incubation of myenteric plexus neurons with CGRP (10(-8) M) in the presence of diltiazem (10(-5) M) or in a calcium-free medium markedly reduced [3H]ACh release. CGRP potentiated [3H]ACh release stimulated by potassium or substance P but not by cholecystokinin octapeptide or forskolin. The results demonstrate that CGRP cause release of ACh from guinea pig myenteric plexus neurons and suggest that the peptide acts through an adenosine 3',5'-cyclic monophosphate-dependent mechanism that involves neuronal calcium channels.

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