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Methods evaluating cannabinoid and endocannabinoid effects on gastrointestinal functions.
Methods Mol Med 2006; 123:169-89MM

Abstract

This chapter briefly describes the physiological neural mechanisms by which diverse neurotransmitter receptor systems control several aspects of gastrointestinal functions such as motility, secretion, feeding, and emesis. The current techniques used to study the effects of cannabinoids on these gastrointestinal functions are then sequentially described, starting with isolated gastrointestinal muscle preparations and ultimately evolving to whole animal models. Both delta9-tetrahydrocannibinol (delta9-THC) and well-studied representatives of other classes of exogenous cannabinoid CB1/CB2 receptor agonists inhibit gastrointestinal motility, peristalsis, defecation, and secretions via cannabinoid CB1 receptors since the CB1 (SR141716A)- and not the CB2 (SR144528)-receptor antagonist reverses these effects in a dose-dependent manner. In addition, exogenous cannabinoids inhibit vomiting produced by diverse emetic stimuli in a SR141716A-sensitive manner in different animal models of emesis. Often these cannabinoids produce hyperphagic effects under laboratory conditions in most human and animal models of feeding. Administration of SR141716A by itself can produce effects opposite to cannabinoid agonists (e.g., increases in gastrointestinal motility and secretions, hyperphagia and vomiting), which suggests an important role for endocannabinoids in these gastrointestinal functions. Indeed, the presence of cannabinoid CB1 receptor markers, endocannabinoids such as anandamide and 2-arachidonoylglycerol (2-AG), their metabolic enzymes, and an endocannabinoid reuptake system have been confirmed in the gastrointestinal tract (GIT). The well-studied endocannabinoid anandamide also seems to reduce both gastrointestinal motility and secretion while producing hyperphagia. On the other hand, while the less well-investigated endocannabinoid 2-AG is a potent emetogen, anandamide may possess weak antiemetic activity.

Authors+Show Affiliations

Department of Basic Medical Sciences, College of Osteopathic Medicine of the Pacific, Western University of Health Sciences, Pomona, CA, USA.

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

16506408

Citation

Darmani, Nissar A.. "Methods Evaluating Cannabinoid and Endocannabinoid Effects On Gastrointestinal Functions." Methods in Molecular Medicine, vol. 123, 2006, pp. 169-89.
Darmani NA. Methods evaluating cannabinoid and endocannabinoid effects on gastrointestinal functions. Methods Mol Med. 2006;123:169-89.
Darmani, N. A. (2006). Methods evaluating cannabinoid and endocannabinoid effects on gastrointestinal functions. Methods in Molecular Medicine, 123, pp. 169-89.
Darmani NA. Methods Evaluating Cannabinoid and Endocannabinoid Effects On Gastrointestinal Functions. Methods Mol Med. 2006;123:169-89. PubMed PMID: 16506408.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Methods evaluating cannabinoid and endocannabinoid effects on gastrointestinal functions. A1 - Darmani,Nissar A, PY - 2006/3/2/pubmed PY - 2006/5/27/medline PY - 2006/3/2/entrez SP - 169 EP - 89 JF - Methods in molecular medicine JO - Methods Mol. Med. VL - 123 N2 - This chapter briefly describes the physiological neural mechanisms by which diverse neurotransmitter receptor systems control several aspects of gastrointestinal functions such as motility, secretion, feeding, and emesis. The current techniques used to study the effects of cannabinoids on these gastrointestinal functions are then sequentially described, starting with isolated gastrointestinal muscle preparations and ultimately evolving to whole animal models. Both delta9-tetrahydrocannibinol (delta9-THC) and well-studied representatives of other classes of exogenous cannabinoid CB1/CB2 receptor agonists inhibit gastrointestinal motility, peristalsis, defecation, and secretions via cannabinoid CB1 receptors since the CB1 (SR141716A)- and not the CB2 (SR144528)-receptor antagonist reverses these effects in a dose-dependent manner. In addition, exogenous cannabinoids inhibit vomiting produced by diverse emetic stimuli in a SR141716A-sensitive manner in different animal models of emesis. Often these cannabinoids produce hyperphagic effects under laboratory conditions in most human and animal models of feeding. Administration of SR141716A by itself can produce effects opposite to cannabinoid agonists (e.g., increases in gastrointestinal motility and secretions, hyperphagia and vomiting), which suggests an important role for endocannabinoids in these gastrointestinal functions. Indeed, the presence of cannabinoid CB1 receptor markers, endocannabinoids such as anandamide and 2-arachidonoylglycerol (2-AG), their metabolic enzymes, and an endocannabinoid reuptake system have been confirmed in the gastrointestinal tract (GIT). The well-studied endocannabinoid anandamide also seems to reduce both gastrointestinal motility and secretion while producing hyperphagia. On the other hand, while the less well-investigated endocannabinoid 2-AG is a potent emetogen, anandamide may possess weak antiemetic activity. SN - 1543-1894 UR - https://www.unboundmedicine.com/medline/citation/16506408/Methods_evaluating_cannabinoid_and_endocannabinoid_effects_on_gastrointestinal_functions_ DB - PRIME DP - Unbound Medicine ER -