Effect of cannabinoids on lithium-induced vomiting in the Suncus murinus (house musk shrew)

Parker, Linda A.; Kwiatkowska, Magdalena; Burton, Page; Mechoulam, Raphael

doi:10.1007/s00213-003-1571-2

Cited by 129 publications

(121 citation statements)

References 35 publications

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“…Indeed, OND also did not suppress the conditioned gaping reactions displayed during re-exposure to the LiCl-paired context . Furthermore, using the emetic species, Suncus murinus (house musk shrew) as an animal model for AN, pre-treatment with a dose of OND that was shown to alleviate acute vomiting (Kwiatkowska et al 2004;Parker et al 2004b), did not reduce the display of conditioned retching reactions during re-exposure to a nausea-paired context . Thus, although OND has proven effective in the reduction of acute post-treatment nausea and vomiting, it does not appear to relieve conditioned nausea when it does develop.…”

Section: Introductionmentioning

confidence: 99%

“…The psychoactive component in marijuanadelta-9-tetrahydrocannabinol (Δ 9 -THC)-has been shown to interfere with the expression of vomiting in shrews and ferrets (Darmani 2001;Parker et al 2004b;Van Sickle et al 2001) and conditioned gaping reactions elicited by a lithium-paired flavor in rats (Limebeer and Parker 1999). The Δ 9 -THC-induced suppression of conditioned nausea could be reversed by a CB 1 receptor antagonist/reverse agonist (SR141716A), implicating the CB 1 receptor in this effect .…”

Section: Introductionmentioning

confidence: 99%

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The effect of cannabidiol and URB597 on conditioned gaping (a model of nausea) elicited by a lithium-paired context in the rat

et al. 2007

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Rationale Anticipatory nausea (AN) experienced by chemotherapy patients is resistant to current anti-nausea treatments. In this study, the effect of manipulation of the endocannabinoid (EC) system on a rat model of nausea (conditioned gaping) was determined. Objective The potential of cannabidiol (CBD) and the fatty acid amide hydrolase (FAAH) inhibitor, URB597 (URB) to reduce conditioned gaping in rats were evaluated. Materials and methods In each experiment, rats received four conditioning trials in which they were injected with lithium chloride immediately before placement in a distinctive odor-laced context. During testing, in experiment 1, rats were injected with vehicle (VEH), 1, 5 or 10 mg/kg CBD 30 min before placement in the context previously paired with nausea and in experiment 2, rats were injected with VEH, 0.1 or 0.3 mg/kg URB 2 h before placement in the context. Additional groups evaluated the ability of the CB 1 antagonist/inverse agonist, SR141716A, to reverse the suppressive effects of URB. Experiment 3 measured the potential of URB to interfere with the establishment of conditioned gaping.Results When administered before testing, CBD (1 and 5, but not 10 mg/kg) and URB (0.3, but not 0.1 mg/kg) suppressed conditioned gaping. The effect of URB was reversed by pre-treatment with the CB 1 antagonist/inverse agonist, SR141716A. When administered before conditioning, URB also interfered with the establishment of conditioned gaping. Conclusions Manipulations of the EC system may have therapeutic potential in the treatment of AN.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The effect of cannabidiol and URB597 on conditioned gaping (a model of nausea) elicited by a lithium-paired context in the rat

et al. 2007

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“…The suppression of Li-induced vomiting by delta9-THC, but not by CBD, was reversed by SR-141716, a CB 1 antagonist, suggesting that both cannabinoids are effective treatments for Li-induced vomiting, however, only delta9-THC acts through the CB 1 receptor. 105 CBD was effective also in the conditioned retching reaction, which is a model of anticipatory nausea. Following three pairings of a novel distinctive contextual cue with the emetic effects of an injection of lithium chloride, the context acquired the potential to elicit conditioned retching in the absence of the toxin.…”

Section: Antiemetic Actionmentioning

confidence: 96%

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Zuardi

2008

Rev. Bras. Psiquiatr.

341

298

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“…Cytotoxic drugs: Cisplatin, cyclophosphamide Intragastric irritants: Copper sulfate, ipecac (Ueno et al, 1987), LiCl (Parker et al, 2004) LiCl (Smith et al, 2001a) Motion ) (Smith et al, 2001a) Radiation (Torii et al, 1993) Nicotine (Ueno et al, 1987) Smith et al, 2001a Hormones and neurotransmitters: Vasopressin (Ikegaya and Matsuki, 2002) a For some stimuli only representative studies or review papers are cited. Only the most common mammalian species used in the study of emesis and malaise are shown.…”

Section: Emesismentioning

confidence: 99%

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

Andrews

Horn

2006

Autonomic Neuroscience

214

200

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Nausea and vomiting are amongst the most common symptoms encountered in medicine as either symptoms of diseases or side effects of treatments. In a more biological setting they are also important components of an organism's defences against ingested toxins. Identification of treatments for nausea and vomiting and reduction of emetic liability of new therapies has largely relied on the use of animal models, and although such models have proven invaluable in identification of the anti-emetic effects of both 5-hydroxytryptamine3 and neurokinin1 receptor antagonists selection of appropriate models is still a matter of debate. The present paper focuses on a number of controversial issues and gaps in our knowledge in the study of the physiology of nausea and vomiting including: The choice of species for the study of emesis and the underlying behavioural (e.g. neophobia), anatomical (e.g. elongated, narrow abdominal oesophagus with reduced ability to shorten) and physiological (e.g. brainstem circuitry) mechanisms that explain the lack of a vomiting reflex in certain species (e.g. rats); The choice of response to measure (emesis[retching and vomiting], conditioned flavour avoidance or aversion, ingestion of clay [pica], plasma hormone levels[e.g. vasopressin], gastric dysrhythmias) and the relationship of these responses to those observed in humans and especially to the sensation of nausea; The stimulus coding of nausea and emesis by abdominal visceral afferents and especially the vagus-how do the afferents encode information for normal postprandial sensations, nausea and finally vomiting?; Understanding the central processing of signals for nausea and vomiting is particularly problematic in the light of observations that vomiting is more readily amenable to pharmacological treatment than is nausea, despite the assumption that nausea represents "low" intensity activation of pathways that can evoke vomiting when stimulated more intensely.

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Effect of cannabinoids on lithium-induced vomiting in the Suncus murinus (house musk shrew)

Cited by 129 publications

References 35 publications

The effect of cannabidiol and URB597 on conditioned gaping (a model of nausea) elicited by a lithium-paired context in the rat

The effect of cannabidiol and URB597 on conditioned gaping (a model of nausea) elicited by a lithium-paired context in the rat

Cannabidiol: from an inactive cannabinoid to a drug with wide spectrum of action

Signals for nausea and emesis: Implications for models of upper gastrointestinal diseases

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