Can you post a reference to where you read this? I'm curious about how exactly they did the experiments
Found Journal on google, have full access as I am university student
article titled:
"From Kratom to mitragynine and its derivatives: Physiological and behavioural
effects related to use, abuse, and addiction"
Neuroscience and Biobehavioral Reviews 37 (2013) 138–151
Pharmacology section - FULL SECTION
11.1.
Receptor interactions
Mitragynine displays a high affinity to (MU)-opioid receptors
(Yamamoto et al., 1999). Also its oxidative derivative, mitragynine
pseudoindoxyl, exhibits potent opioid agonistic properties in
vitro. Pharmacological investigations have shown that mitragynine
acts at supraspinal- (MU) and (DELTA)-opioid receptors for its antinociceptive
effects (Matsumoto et al., 1996a; Tohda et al., 1997;
Thongpradichote et al., 1998). However, for other psychoactive
effects, central opioid receptors may be more relevant. The affinity
of mitragynine to (MU)- and (KA)-opioid receptors is considerably lower,
but higher than that of morphine. It was shown that the methoxy
group at the C9 position as well as the Nb lone electron pair in the
fundamental structure are essential for the opioid agonist activity
(Takayama et al., 2002; Taufik Hidayat et al., 2010). A high opioid
receptor potency was found for the minor M. speciosa constituent 7-
HMG, suggesting full agonist properties.
Kratom powder was found
to have a 350-fold less affinity to the (MU)-opioid receptor than morphine
in a 3H-[D-Ala2,N-MePhe4, Gly-ol]-enkephalin(3H-DAMGO)
radioligand binding assay in HEK 293 cells (Havemann-Reinecke,
2011).
11.2.
Cellular effects
At cellular level, mitragynine inhibits neurotransmitter release
from the nerve endings at the vas deferens, partly through the
blockade of neuronal Ca2+ channels (Matsumoto et al., 2005b).
The authors proposed the neuronal Ca2+ channel-blocking effect
of mitragynine as a general mechanism for the analgesic and other
physiological actions of mitragynine. In addition, mitragynine was
shown to inhibit forskolin-stimulated cAMP formation in NG108-
15 cells in vitro. This effect could be blocked by the opioid receptor
antagonist naloxone, but not by the alpha-2-adrenoceptor antagonist
idazoxane (Tohda et al., 1997).
I would have thought it would have a-2-agonist action like clonidine, which adds pain-relief, since it is structurally shaped similar to an a-2-antagonist yhoimbe