Year: 2008
Type: article
Abstract: Although opioids are known to have a local analgesic action by nerve conduction block, it remains to be unclear whether this action is due to opioid-receptor activation. We have previously reported that a non-narcotic opioid tramadol more effectively inhibits compound action potentials (CAPs) than its metabolite mono-O-demethyl-tramadol (M1) in a manner independent of opioid-receptor activation and that this difference in inhibition between the two opioids may be due to a distinction between their chemical structures. To address further this issue, we examined the effects of opioids (morphine, codeine, ethylmorphine and dihydrocodeine) and cocaine on CAPs by applying the air-gap method to frog sciatic nerves. All of the opioids at concentrations less than 10 mM reduced the peak amplitude of the CAP in a reversible and dose-dependent manner; this action was resistant to a nonspecific opioid-receptor antagonist naloxone. The sequence of the CAP peak amplitude reductions was ethylmorphine (IC50 = 4.6 mM) > codeine > dihydrocodeine ≥ morphine; this opioid-mediated inhibition was much less than that of cocaine (IC50 = 0.80 mM). The CAP peak amplitude reductions produced by morphine, codeine and ethylmorphine were related to their chemical structures in such that this extent enhanced with an increase in the number of -CH2 in a benzene ring, as seen in the inhibitory actions of tramadol and M1. It is suggested that the substituted groups of -OH bound to the benzene ring of morphine, codeine and ethylmorphine as well as tramadol and M1 may play an important role in producing nerve conduction block.
Source: PAIN RESEARCH
DOI: 10.11154/pain.23.185
Language: English
Subfield: Surgery
Field: Medicine
Domain: Health Sciences
Open Access status: diamond
OpenAlex ID: W2333600752