Octopamine-mediated neuronal plasticity in honeybees: implications for olfactory dysfunction in humans.

Biogenic amines, such as norepinephrine (in vertebrates) and octopamine (in invertebrates), have structural and functional similarities. These amines play crucial roles in animal behavior by modifying the synaptic output of relevant neurons. Increased levels of norepinephrine in the olfactory bulb preferentially increase mitral cell excitatory responses to olfactory nerve inputs, suggesting its critical role in modulating olfactory function including memory formation and/or recall of specific olfactory memories. Increased levels of octopamine in the antennal lobe play an important role in a reinforcement pathway involved in olfactory learning and memory in honeybees. Similar to adrenergic receptors in the human brain, activation of octopaminergic receptors in the honeybee brain induces specific second messenger pathways that change protein phosphorylation and/or gene expression, altering the activity and/or abundance of proteins responsible for neuronal signaling leading to changes in olfactory behavior. The author's studies in honeybees Apis mellifera indicate that oxidative stress plays a major role in olfactory dysfunction. A similar mechanism has been proposed for olfactory abnormalities in patients of Alzheimer disease and Parkinson disease. Due to similarities in cellular and molecular processes, which govern neuronal plasticity in humans and honeybees, the author proposes that the honeybee can be used as a potential and relatively simple model system for understanding human olfactory dysfunction during aging and in neurodegenerative diseases.