Synergistic interactions of endogenous opioids and cannabinoid systems
Cannabinoids are a range of naturally occurring chemical compounds that are exclusive to the cannabis plant. The effects of the marijuana plant (cannabis sativa), when smoked, is said to give you a stoned feeling. Cannabinoids include two main chemicals and these are tetrahydrocannabinol (THC) and cannabidiol (CBD).
THC is the psychotropic part of cannabis and it is responsible for giving the user irrational thoughts. CBD is the calming agent in marijuana and is said to give off a neuroprotective and anti inflammatory effects on its users. CBD is one of the major cannabinoids and CBD has been shown to cure nausea and vomiting arising from a range of human conditions. The endocannabinoid system is the network in which cannabinoids can thrive via the cannabinoid receptors 1 and 2. This paper will have a look into the collegial relationship between endogenous cannabinoids and their respective system in which they are allowed to work.
Cannabinoids are individualistic drug types historically applied in combination to cure chronic pain. THC, a working part in marijuana, releases endogenous dynorphin A and leucine enkephalin in the makings of therapeutic agents. The endogenous cannabinoid, anandamide AEA , unsuccessfully expels dynorphin A. The synthetic cannabinoid, CP55,940, expels dynorphin B. Neither AEA nor CP55,940 enhances morphine analgesia. The CB1 antagonist, SR141716A, differentially prevents THC versus AEA. Resistance to THC, but not AEA, includes a reduction in the expulsion of dynorphin A. this preclinical research suggests that THC and morphine can be applicable in low dose mixtures as a therapeutic. This is never seen with AEA or CP55,940.
Scientists here flirt with the idea of the being of a fresh cannabinoid receptor contrasting in nature than the endogenous opioid networks based upon results displaying the stereoselectivity of endogenous opioid expulsion. Such a receptor, because of the expulsion of endogenous opioids, might have massive effects upon the clinical advancement of cannabinoid and opioid mixtures for the therapeutic of numerous bouts of chronic pain in humans
Overall, it has been illustrated that THC and levonantradol increase the antinociceptive impacts of morphine. THC expels dynorphin A, but levonantradol expels dynorphin B. CP55 and AEA do not increase the impacts of morphine spinally. CP55 expels dynorphin B. AEA expels no opioid peptides. Antinociceptive impacts of THC, levonantradol, CP55, and AEA are all prevented by the CB1 antagonist, SR141716A. Thus, four individualised cannabinoids put force on four different systems of a relationship or no relationship between endogenous opioid networks.
The scientists in this research have gone on to say that such a diversity of relationships might be indicative of cannabinoid receptor 1 sub categories in the spinal cord. Such sub categories might be clinically detrimental in the growth or application of cannabinoids in the curing of chronic pain.