The cannabinoid antagonist SR144528 enhances the acute effect of WIN 55,212‐2 on gastrointestinal motility in the rat

@article{Abalo2010TheCA,
  title={The cannabinoid antagonist SR144528 enhances the acute effect of WIN 55,212‐2 on gastrointestinal motility in the rat},
  author={Raquel Abalo and Pablo Antonio Cabezos and Gema Vera and R. Fern{\'a}ndez‐pujol and M. I. Martı́n},
  journal={Neurogastroenterology \& Motility},
  year={2010},
  volume={22}
}
Background  In the absence of pathology, cannabinoid‐induced depression of gastrointestinal (GI) motility is thought to be mediated primarily by CB1 receptors, whereas the role of CB2 receptors is still unclear. The aim of this work was to radiographically analyze the acute effect of the mixed cannabinoid agonist WIN 55,212‐2 (WIN) on GI motor function in the rat, focusing on the involvement of CB1 and CB2 receptors. 
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TLDR
The fact that AM251, but not AM630, is capable of reducing the effect of vincristine suggests that, like in other experimental models of paralytic ileus, an increased cannabinoid tone develops and is at least partially responsible for the alterations induced by the antitumoral drug on gastrointestinal motor function.
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References

SHOWING 1-10 OF 48 REFERENCES
Selective lack of tolerance to delayed gastric emptying after daily administration of WIN 55,212‐2 in the rat
  • R. Abalo, P. A. Cabezos, M. Martı́n
  • Biology, Medicine
    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
  • 2009
TLDR
The different systems show differential sensitivity to cannabinoids and tolerance developed at different rates, with delayed gastric emptying being particularly resistant to attenuation upon chronic treatment.
Inhibitory effect of cannabinoid agonists on gastric emptying in the rat
TLDR
It is suggested that cannabinoid agonists delay gastric emptying through activation of cannabinoid CB1 receptors, while the endogenous cannabinoid system does not seem to modulate gastric motility.
Effects of cannabinoid receptor‐2 activation on accelerated gastrointestinal transit in lipopolysaccharide‐treated rats
TLDR
The activation of CB2 receptors in response to LPS is a mechanism for the re‐establishment of normal gastrointestinal transit after an inflammatory stimulus.
The role of central and peripheral Cannabinoid1 receptors in the antihyperalgesic activity of cannabinoids in a model of neuropathic pain.
TLDR
Cannabinoids are highly potent and efficacious antihyperalgesic agents in a model of neuropathic pain and are likely to be mediated via an action in the CNS and in the periphery.
Activation of cannabinoid CB1 and CB2 receptors suppresses neuropathic nociception evoked by the chemotherapeutic agent vincristine in rats
The ability of cannabinoids to suppress mechanical hypersensitivity (mechanical allodynia) induced by treatment with the chemotherapeutic agent vincristine was evaluated in rats. Sites of action were
Involvement of cannabinoid receptors in inflammatory hypersensitivity to colonic distension in rats
  • M. Sansón, L. Buéno, J. Fioramonti
  • Biology, Medicine
    Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society
  • 2006
TLDR
It is concluded that colonic inflammation enhances the antinociceptive action of CB1 and CB2 receptor agonists, and activates an endogenous, CB1 receptor mediated, antinOCiceptive pathway.
...
...