Inhibition by indomethacin of naloxone-precipitated opiate withdrawal contraction in isolated guinea pig myenteric plexus-longitudinal muscle preparation

Life Sciences ◽  
1986 ◽  
Vol 39 (3) ◽  
pp. 243-247 ◽  
Author(s):  
Marc S. Krakow ◽  
Eli D. Ehrenpreis ◽  
Seymour Ehrenpreis
1981 ◽  
Vol 59 (3) ◽  
pp. 307-310 ◽  
Author(s):  
K. Jhamandas ◽  
J. Elliott ◽  
M. Sutak

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.


1975 ◽  
Vol 53 (4) ◽  
pp. 566-574 ◽  
Author(s):  
John C. Szerb

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.


1998 ◽  
Vol 76 (3) ◽  
pp. 340-346 ◽  
Author(s):  
Angela A Coutts ◽  
Roger G Pertwee

Cannabinoid receptor agonists inhibit electrically evoked isometric contractions of the myenteric plexus - longitudinal muscle preparation of the guinea-pig small intestine (MPLM), probably by reducing release of acetylcholine (ACh) through the activation of prejunctional CB1 receptors. As CB1 receptors are thought to be negatively coupled through Gi/o proteins to both N-type Ca2+ channels and adenylate cyclase, we have now further investigated the involvement of CB1 receptors by monitoring the effects of forskolin, 8-bromo-cAMP, 3-isobutyl-1-methylxanthine (IBMX), and extracellular Ca2+ on the ability of the cannabinoid agonist, (+)-WIN 55212 to inhibitelectrically evoked contractions of the MPLM (0.1 Hz, 0.5.ms, and 110% maximal voltage). Some experiments were performed with normorphine instead of (+)-WIN 55212. At 10-7 M, forskolin, 8-bromo-cAMP, and IBMX were found to reduce significantly the maximum inhibitory response to (+)-WIN 55212 by 49.4, 48.4, and 40.2%, respectively, without affecting control contractions or responses to exogenous ACh. Low external Ca2+ (0.64 mM) significantly increased the maximum response to (+)-WIN 55212 and shifted the curve slightly leftwards, whereas high external Ca2+ (5.08 mM) reduced the maximum response by 27.2%. The concentration-response curve to normorphine, which also reduces evoked contractions of this preparation as a result of a presynaptic inhibition of ACh release via opioid µ receptors, was affected similarly. These results support the hypothesis that cannabinoid-induced inhibition in the MPLM is mediated by CB1 receptors.Key words: cannabinoid, myenteric, calcium, cAMP, normorphine.


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