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.

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.

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.

BaCl2-induced contractions in the guinea pig ileum longitudinal muscle: role of presynaptic release of neurotransmitters and Ca2+ translocation in the postsynaptic membrane

1981 ◽  
Vol 59 (6) ◽  
pp. 541-547 ◽  
Author(s):  
John G. Clement
Keyword(s):  
Substance P ◽  
Guinea Pig ◽  
Longitudinal Muscle ◽  
Postsynaptic Membrane ◽  
Muscle Membrane ◽  
Guinea Pig Ileum ◽  
Presynaptic Neuron ◽  
Smooth Muscle Membrane ◽  
Release Of Acetylcholine ◽  
The Right

Early studies indicated that the BaCl2-induced contractions in the guinea pig ileum longitudinal muscle strip (GPI-LMS) were, in part, neuronal in origin. However, recent studies have suggested that BaCl2-induced contractions were produced by an action directly on the smooth muscle membrane. The purpose of this study was to investigate the mechanism of the BaCl2 contractions in the GPI-LMS. Botulinum toxin (5 × 105 MLD/mL), which blocks the electrically induced release of acetylcholine (ACh), hemicholinium-3 (HC-3; 110 μM), which blocks ACh synthesis, tetrodotoxin (TTX; 60 nM), which blocks Na+ channels, black widow spider venom, which depletes the presynaptic neuron of neurotransmitter, and atropine (2.9 μM), a potent muscarinic antagonist, had no effect on the BaCl2 contractions. Desensitization of the GPI-LMS to substance P did not affect the BaCl2 contraction. In Ca2+-free buffer the BaCl2 dose–response curve was shifted to the right. In Ca2+-free solution the time to 50% inhibition of the contractile response to ACh (73 nM) and BaCl2 (1.16 mM) was 3.7 and 125 min, respectively. The D 600 IC50 for ACh and BaCl2 contractions was 220 and 130 nM, respectively. In Ca2+-free buffer either EGTA (0.53 mM) or D 600 (1 μM) were potent inhibitors of BaCl2 contractions. These results suggest that in the GPI-LMS the BaCl2 response is not mediated by a release of ACh (or substance P) because inhibitors of ACh release, synthesis, and receptors do not affect the responses. Also, the BaCl2 contraction is not due to activation of Na+ channels because TTX is without effect. The BaCl2-induced contraction appears to be mainly due to the movement of membrane bound Ca2+ through D 600 sensitive Ca2+ channels with extracellular Ca2+ and possible passage of Ba2+ ions intracellularly playing relatively minor roles.

PACAP is a stimulator of neurogenic contraction in guinea pig ileum

1993 ◽  
Vol 265 (2) ◽  
pp. G295-G302 ◽  
Author(s):  
S. Katsoulis ◽  
A. Clemens ◽  
H. Schworer ◽  
W. Creutzfeldt ◽  
W. E. Schmidt
Keyword(s):  
Biological Activity ◽  
Substance P ◽  
Guinea Pig ◽  
Adrenergic Blockade ◽  
Guinea Pig Ileum ◽  
Pituitary Adenylate Cyclase ◽  
Release Of Acetylcholine ◽  
High Sequence Homology ◽  
Derivatives Of

The myotropic effect of pituitary adenylate cyclase-activating polypeptide (PACAP), a novel brain-gut peptide with high sequence homology to vasoactive intestinal polypeptide (VIP), was studied in the isolated guinea pig ileum in vitro. PACAP contracts the guinea pig ileum significantly more potently and efficiently compared with VIP. PACAP-induced contraction was abolished by tetrodotoxin, dynorphin, and somatostatin, partially reduced by atropine, and not affected by ganglionic and adrenergic blockade. The atropine-resistant component was sensitive to spantide, to the induction of tachyphylaxis with substance P, and to omega-conotoxin. Ileal strips desensitized to PACAP did not respond to VIP, although they maintained their sensitivity to PACAP after desensitization to VIP. COOH-terminal-truncated derivatives of PACAP exhibited full biological activity, although some of them showed substantially reduced potency. Deletion of NH2-terminal amino acids abolished biological activity. PACAP produced a concentration-dependent increase in the release of [3H]acetylcholine from longitudinal muscle-myenteric plexus preparations preloaded with [3H]choline. This effect was Ca2+ dependent, tetrodotoxin sensitive, and resistant to hexamethonium and scopolamine. In contrast, PACAP inhibited release of acetylcholine evoked by field stimulation. In summary, PACAP-induced contraction of the guinea pig ileum is mediated via release of acetylcholine and substance P through interaction with PACAP-1 and VIP/PACAP-2 receptors. PACAP has to be added to the list of myotropic neuropeptides of the gastrointestinal tract.

Properties of synaptic inputs from myenteric neurons innervating submucosal S neurons in guinea pig ileum

2000 ◽  
Vol 278 (2) ◽  
pp. G273-G280 ◽  
Author(s):  
B. A. Moore ◽  
S. Vanner
Keyword(s):  
Guinea Pig ◽  
Myenteric Plexus ◽  
Intracellular Recordings ◽  
Guinea Pig Ileum ◽  
Myenteric Neurons ◽  
Synaptic Inputs ◽  
Stimulus Train ◽  
Stimulation Of ◽  
Double Chamber

This study examined synaptic inputs from myenteric neurons innervating submucosal neurons. Intracellular recordings were obtained from submucosal S neurons in guinea pig ileal preparations in vitro, and synaptic inputs were recorded in response to electrical stimulation of exposed myenteric plexus. Most S neurons received synaptic inputs [>80% fast (f) excitatory postsynaptic potentials (EPSP), >30% slow (s) EPSPs] from the myenteric plexus. Synaptic potentials were recorded significant distances aboral (fEPSPs, 25 mm; sEPSPs, 10 mm) but not oral to the stimulating site. When preparations were studied in a double-chamber bath that chemically isolated the stimulating “myenteric chamber” from the recording side “submucosal chamber,” all fEPSPs were blocked by hexamethonium in the submucosal chamber, but not by a combination of nicotinic, purinergic, and 5-hydroxytryptamine-3 receptor antagonists in the myenteric chamber. In 15% of cells, a stimulus train elicited prolonged bursts of fEPSPs (>30 s duration) that were blocked by hexamethonium. These findings suggest that most submucosal S neurons receive synaptic inputs from predominantly anally projecting myenteric neurons. These inputs are poised to coordinate intestinal motility and secretion.

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