The Neurobiology of Placebo Effects
Hanna Pickard, Serge H. Ahmed in The Routledge Handbook of Philosophy and Science of Addiction, 2019
Following the exposure to nonopioid drugs the placebo response is not mediated by mu opioid receptors but by the CB1 cannabinoid receptors. Indeed, when the nonopioid drug ketorolac is administered for two consecutive days and then replaced with a placebo on the third day, the placebo analgesic response is not reversed by naloxone. However, the CB1 cannabinoid receptor antagonist, rimonabant, blocks this placebo analgesic response completely (Benedetti et al. 2011b). Moreover, the whole lipidic pathway, involving arachidonic acid, endogenous cannabinoid ligands (e.g., anandamide), and the synthesis of prostaglandins and thromboxane, seems to be important in the modulation of the placebo response in pain. In particular, cyclooxygenase, which is involved in prostaglandins and thromboxane synthesis, has been found to be modulated by both placebo and nocebo in hypobaric hypoxia headache (Benedetti et al. 2014).
Herbal Cannabinomimetics
Amritpal Singh Saroya in Reverse Pharmacology, 2018
The plant is popularly known as eastern purple cone flower. In rat brain membrane preparations, the bioactivity of three alkamides and nitidanin diisovalerianate from E. purpurea were studied in [35S]GTPyS-binding experiments. The compounds showed partial as well as inverse agonist compounds for cannabinoid (CB1) receptors. This was proved by weak to moderate interactions mechanisms involved in the G-protein signaling mechanisms. However, when coadministered with arachidonyl- 2’-chloroethylamide (a synthetic agonist of the cannabinoid receptor1 CB1R), the compounds inhibited the stimulation of the pure agonist. This clearly demonstrates cannabinoid receptor antagonist properties (Hohmann et al. 2011).
Herbs with Antidepressant Effects
Scott Mendelson in Herbal Treatment of Major Depression, 2019
In several studies, antidepressant-like effects were noted. Salvinorin A reduced immobility in the forced swim test with rats, and in the tail suspension test with mice. These effects could be blocked by either the κ-opioid receptor antagonist nor-binaltorphimine or the CB1 cannabinoid receptor antagonist AM251. Treatment with Salvinorin A also suggested anxiolytic effects in rats in the elevated plus maze.11 Chronic treatment of rats with salvinorin A also reversed the reduction in preference for sucrose – considered a form of depression-like anhedonia – that was induced by chronic unpredictable stress.12
Naltrexone at low doses (LDN) and its relevance to cancer therapy
Published in Expert Review of Anticancer Therapy, 2022
The activation of the central signaling pathways is not an effect unique to any one of the opioid receptors, but most likely a generic feature of GPCR activation. Similarly, binding through these receptors can be promiscuous, with multiple ligands capable of binding to many receptors with varying affinities. Furthermore, this plasticity in ligand binding is not limited to binding to the opioid receptor. For example, the chronic administration of the cannabinoid receptor antagonist SR141716A can modify the action of the opioid receptors [8], through a spill-over effect of the cannabinoid into the semi-homologous opioid receptor. Similarly, morphine can elicit a physiological response by cross-reacting with the somatostatin receptor [9]. Taken together, it is easy to see how exogenous sources of opioids and their related compounds could modify the natural functions of ligand-receptor systems in the body; a number of which may not be canonical.
Cannabis as a potential compound against various malignancies, legal aspects, advancement by exploiting nanotechnology and clinical trials
Published in Journal of Drug Targeting, 2022
Nazeer Hasan, Mohammad Imran, Afsana Sheikh, Suma Saad, Gaurav Chaudhary, Gaurav Kumar Jain, Prashant Kesharwani, Farhan J. Ahmad
Many research groups have been investigated cannabinoids against pancreatic cancer. After the investigation by RT-PCR, both CB1 and CB2 receptors were present on pancreatic carcinoma cells. Cannabinoid and its component mark the anti-cancer event, such as apoptosis, migration, and proliferation by manipulating the blood vessel morphology and decreasing blood vessel tumour activation factor-like vascular endothelial growth factor. Nevertheless, the effect varies between different cancers [139]. Cannabinoid, due to upregulation of ATF-4, p8, and TRB3 stress-related genes, leads to apoptosis in pancreatic cancer cells [140]. In another study by Fogli et al., AM251, a cannabinoid receptor antagonist showed cell death in MIAPaCa-2 cells through a receptor-independent manner [141].
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