Pain relief of cannabinoids in the KATP pathway and its connections to the opioid pathway in mice

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Pain relief of cannabinoids in the KATP pathway and its connections to the opioid pathway in mice

Published Date

2019

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Scholarly Text or Essay

Abstract

Opioids are known to be addictive drugs, and long term use may lead to overdose or death. To combat the opioid epidemic, different therapies should be developed and used for pain management. One potential alternative to prescription opioids is cannabis. The science of cannabinoids, the chemical compounds in cannabis, is relatively new research. There are two primary cannabinoid receptors: CB1 and CB2, both being G protein coupled receptors (Pertwee, 2006). The receptors are especially sensitive to THC and cannabidiol, both components in cannabis, which are thought to aid in pain relief. The hypothesized pathway begins with a cannabinoid binding to its receptor, which inhibits adenylyl cyclase. Adenylyl cyclase is responsible for producing cyclic adenylyl phosphate (cAMP) from ATP. Inhibiting adenylyl cyclase decreases the concentration of cAMP, resulting in the opening of ATP sensitive potassium channel opening (K ATP channels, Pertwee, 2006). This aligns with an accepted pathway for opioid signal transduction (Figure 2), and it is possible cannabinoids and opioids affect the same downstream potassium channels. In this research, experimentation of mice was used to observe the potassium channel connections between the opioid and cannabinoid pathways. This was the starting point in finding a potentially safer therapy than opioids but with similar pain relief efficacy.

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University Honors Capstone Project Paper and Poster, University of Minnesota Duluth, 2019. Department of Pharmacy Practice and Pharmaceutical Sciences. Faculty mentor: Amanda Klein.

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Messerschmidt, Lauren; Klein, Amanda. (2019). Pain relief of cannabinoids in the KATP pathway and its connections to the opioid pathway in mice. Retrieved from the University Digital Conservancy, https://hdl.handle.net/11299/203639.

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