Solving Cannabis Hyperemesis Syndrome | How Cannabinoids Regulate Nausea | FPS#5

Why do cannabinoids in cannabis cause nausea and vomiting in some people but not others? Is this limited to heavy users, Recreational users, medicinal cannabis patients? In this episode, FPS ventures into the unknown on the very under-researched area of Cannabinoid Hyperemesis Syndrome. In this episode neuroscience PhD candidate Marieka Devuono joins us to speak about her recently published manuscript that addresses these controversial concepts, entitled "Conditioned gaping produced by high dose Δ9-tetrahydracannabinol: Dysregulation of the hypothalamic endocannabinoid system", published in Neurophamacology [2018 Oct;141:272-282. doi: 10.1016/j.neuropharm.2018.08.039].
Link: https://linkinghub.elsevier.com/retrieve/pii/S0028-3908(18)30598-7

Highlights
• High doses of THC produce nausea-induced conditioned gaping.
• THC-induced conditioned gaping was mediated by its action on the CB1 receptor.
• 10 mg/kg THC produced upregulation of genes related to the 2-AG degrading enzyme, MAGL in the hypothalamus.
• High doses of THC may produce stress-induced nausea by dysregulation of endocannabinoid function in the hypothalamus.

Abstract
Δ9-tetrahydracannabinol (THC) is recognized as an effective treatment for nausea and vomiting via its action on the cannabinoid 1 (CB1) receptor. Paradoxically, there is evidence that THC can also produce nausea and vomiting. Using the conditioned gaping model of nausea in rats, we evaluated the ability of several doses of THC (0.0, 0.5, 5 and 10 mg/kg, i.p.) to produced conditioned gaping reactions. We then investigated the ability of the CB1 receptor antagonist, rimonabant, to block the establishment of THC-induced conditioned gaping. Real-time polymerase chain reaction (RT-PCR) was then used to investigate changes in endocannabinoid related genes in various brain regions in rats chronically treated with vehicle (VEH), 0.5 or 10 mg/kg THC. THC produced dose-dependent gaping, with 5 and 10 mg/kg producing significantly more gaping reactions than VEH or 0.5 mg/kg THC, a dose known to have anti-emetic properties. Pre-treatment with rimonabant reversed this effect, indicating that THC-induced conditioned gaping was CB1 receptor mediated. The RT-PCR analysis revealed an upregulation of genes for the degrading enzyme, monoacylglycerol lipase (MAGL), of the endocannabinoid, 2-arachidolyl glycerol (2-AG), in the hypothalamus of rats treated with 10 mg/kg THC. No changes in the expression of relevant genes were found in nausea (interoceptive insular cortex) or vomiting (dorsal vagal complex) related brain regions. These findings support the hypothesis that THC-induced nausea is a result of a dysregulated hypothalamic-pituitary-adrenal axis leading to an overactive stress response.

Keywords
THC Conditioned gaping Endocannabinoid system Hypothalamus Nausea.

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