Remifentanil reduces glutamate toxicity in rat olfactory bulb neurons in culture

Abstract

Background

Opioids are widely used as an analgesic drug in the surgical setting. Remifentanil is an ultra-short acting opioid with selective affinity to the mu (µ) receptor, and also exhibits GABA agonist effects. The aim of this study was study of the neurotoxic or neuroprotective effect of different doses of remifentanil in glutamate-induced toxicity in olfactory neuron cell culture.

Materials and methods

Olfactory neurons were obtained from newborn Sprague Dawley rat pups. Glutamate 10^-5 mM was added to all culture dishes, except for the negative control group. Remifentanil was added at three different doses for 24 hours, after which evaluation was performed using 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), Total Antioxidant Capacity (TAC), Total Oxidant Status (TOS), and Annexin V.

Results

The highest and lowest viability values were obtained from the low and high remifentanil doses at approximately 91% and 75%, respectively. TAC and TOS were correlated with the MTT results. TAC, TOS and MTT most closely approximated to the sham group values in the remifentanil 0.02 mM group.

Conclusions

Our results suggest that remifentanil has the potential to reduce glutamate toxicity and to increase cell viability in cultured neuron from the rat olfactory bulb.

KEYWORDS
Remifentanil; Olfactory bulb neuron; Glutamate; Neurotoxicity