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Cannabinoids are found in the marijuana plant (cannabis sativa) and are said to be effective in pain management from pain symptoms such as multiple sclerosis, act as an anti-inflammatory, diabetic neuropathy, peripheral neuropathy and nausea and vomiting. A cannabinoid is one of a great collection of complex chemical compounds that naturally occur in the body and operates on major cannabinoid receptors in cells that mediates neurotransmitter release in the brain.
Cannabinoids for these receptors include the endocannabinoid system. The main cannabinoid is the phytocannabinoid tetrahydrocannabinol (THC), the primary psychoactive chemical that is found in the cannabis plant. Cannabidiol (CBD) is another main constituent of the plant and produces a non-psychotic effect. This paper will look at the role of cannabinoids in pain regulation.
In animals, numerous people of the Transient Receptor Potential network family (TRPs), communicated majorly in the sensory neurons and skin keratinocytes, are prevented in significant physiological abilities, including thermosensation, nociception and vision. Since the TRPV1-4, TRPA1 and TRPM8 networks from this family play a massive role in both the detection and potentially changing of hurtful stimuli, they are seen as quite a plausible target of novel therapeutic agents.
A few agents playing at TRPs, such as capsaicin or menthol, have a long past of their utility as therapeutic, whereas others are now being reviewed both in animals and in humans. In this evaluation, pain physiology is talked about, as well as the pharmacological abilities of the TRPs in cahoots with pain detection as a plausible crucial peripheral therapeutic targets. We present one of the most relevant strategies in the search for novel analgesic drugs, namely the TRP networks and their cannabinoids, both agonists and antagonists as possible standard analgesics for inflammatory and neuropathic pain disorders.
Cannabinoids may be utilised as an anti-inflammatory agent. In fact, human TRP subfamilies involve members that underlie numerous other diseases in humans, such as ‘amyotrophic lateral sclerosis and parkinsonism-dementia (TRPM2), hypomagnesemia and hypocalcemia (TRPM6), kidney diseases (TRPP2, TRPC6), skeletal diseases and neuropathies (TRPV4), progressive familial heart block type I (TRPM4) and childhood neurodegenerative disease (TRPML1)’. These syndromes are quoted from the paper in which this article is based. This understanding is also a great challenge for the growth of novel agents for the treatment of these disorders.