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Mechanism Of Myercene And How It Is So Distinctive In Pain Management

Myrcene has a direct analgesic effect similar to that described for peripheral acting opiates or dipyrone. Myrcene appears as a potentially safer alternative to other analgesic applications, all of which are associated with major toxicological problems. Terpenes such as myrcene may constitute a lead for the development of new peripheral analgesics with a profile of action different from that of the aspirin-like drugs

Myrcene, a monoterpene has been investigated for antinociception in mice by a low temperature (51.5 +/- 0.5 degrees C) hot plate method and by the acetic acid-induced writhing test. Significant inhibition of nociception was seen in the tests with myrcene at doses of 10 and 20 mg kg-1 (i.p.) or at 20 and 40 mg kg-1 (s.c.), respectively. The antinociceptive effect was significantly antagonized by naloxone (1 mg kg-1) or yohimbine (2 mg kg-1). The results suggest that myrcene is capable of inducing antinociception in mice, probably mediated by alpha 2-adrenoceptor stimulated release of endogenous opioids.

By the mid-1960s, it had become apparent from pharmacological studies that opiate drugs were likely to exert their actions at specific receptor sites, and that there were likely to be multiple such sites.[4] Early studies had indicated that opiates appeared to accumulate in the brain.[5] The receptors were first identified as specific molecules through the use of binding studies, in which opiates that had been labeled with radioisotopes were found to bind to brain membrane homogenates. The first such study was published in 1971, using 3H-levorphanol.[6] In 1973, Candace Pert and Solomon H. Snyder published the first detailed binding study of what would turn out to be the μ opioid receptor, using 3H-naloxone.[7] That study has been widely credited as the first definitive finding of an opioid receptor, although two other studies followed shortly after

Reduction or inhibition of neurotransmission, due largely to opioid-induced presynaptic inhibition of neurotransmitter release.Involves changes in transmembrane ion conductance.Increase potassium conductance (hyperpolarization).Inactivation of calcium channels

Activation of peripheral nociceptive fibers causes release of substance P and other pain-signaling neurotransmitters from nerve terminals in the dorsal horn of the spinal cord

Release of pain-signaling neurotransmitters are regulated by endogenous endorphins or by exogenous opioid agonists by acting presynaptically to inhibit substance P release, causing analgesia

Myrcene is analgesic, and such activity, in contrast to cannabinoids, is blocked by naloxone (Rao et al 1990), suggesting an opioid-like mechanism. It also blocks inflammation via PGE-2 (Lorenzetti et al 1991)

Unlike narcotic related drugs Myrcene does not germinate tolerance in the body for the drugs itself and can recommend for, as strong as opiate and dipyrone like pain management. 



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