Iron-induced oxidative stress modulates olfactory learning and memory in honeybees.

Abstract

Reactive oxygen species (ROS)-mediated oxidative stress tends to increase with environmental stress, aging, and age-related diseases resulting in progressive neuronal dysfunction. The purpose of the present study was to examine whether or not oxidative stress can be induced into the antennal lobes of the honeybee brain by injecting ferrous ammonium citrate (FAC). Proboscis Extension Reflex conditioning procedure was used to assay subjects' responses to odorants for evaluating the effect of oxidative stress on the olfactory learning and memory. FAC-induced inhibitory effect on olfactory learning and memory was dose-and time-dependent. Injections of reduced glutathione (GSH) into the antennal lobes before FAC treatment blocked oxidative stress-mediated inhibitory effect. Injections of VK-28 prior to FAC treatment overcame oxidative stress-mediated inhibitory response. However, injections of GSH into the antennal lobes prior to mianserin/dsRNA treatment did not reverse octopamine receptor disruption-mediated inhibitory response. These results indicate that normal cellular redox is crucial for olfactory processing, and chelation of iron prevents ROS-mediated oxidative stress. Furthermore, octopamine receptor disruption, and FAC-mediated oxidative stress confer two independent mechanisms that impair olfactory learning and memory in honeybees.