Fentanyl increases catecholamine oxidation current measured by in vivo voltammetry in the rat striatum.

Abstract

A proposed mechanism for fentanyl-induced muscular rigidity is the effect of opioids on dopaminergic transmission in the striatum. The objective of this study was to observe the effect of fentanyl on the rat striatal catechol oxidation current (CA.OC) which reflects extracellular DOPAC (3-4,dihydroxyphenylacetic acid) concentration (a major metabolite of dopamine), as measured by in vivo voltammetry. Male Sprague-Dawley rats, anaesthetized with halothane, were stereotaxically implanted with carbon fibre electrodes in the striatum and after an initial stabilization period of an hour were given a control saline IV injection followed 30 min later by fentanyl 10 micrograms.kg-1 IV over 10 min and at 70 min by the monoamine oxidase inhibitor pargyline 70 mg.kg-1 IP. Fentanyl produced a significant (P less than 0.05 Anova) increase in CA.OC in all animals. This reached a plateau 15 min following the administration of fentanyl and was at a maximum of 148 +/- 10.2 per cent of control 35 min after the administration of fentanyl. Pargyline produced a rapid decline in CA.OC peak height which went from 143 +/- 11.6 to 39 +/- 6.8 per cent of control over 30 min. There were no significant differences between the pH, PaO2 and PaCO2 during the saline and fentanyl injection periods and there was no significant variation of blood pressure throughout the experiment. This study shows that under stable physiological conditions, fentanyl produces a significant increase in CA.OC in the rat striatum.