Abstract
Cocaine, a potent addictive substance, is an inhibitor of monoamine transporters, including DAT (dopamine transporter), SERT (serotonin transporter) and NET (norepinephrine transporter). Cocaine administration induces complex behavioral alterations in mammals, but the underlying mechanisms are not well understood. Here, we tested the effect of cocaine on C. elegans behavior. We show for the first time that acute cocaine treatment evokes changes in C. elegans locomotor activity. Interestingly, the neurotransmitter serotonin, rather than dopamine, is required for cocaine response in C. elegans. The C. elegans SERT MOD-5 is essential for the effect of cocaine, consistent with the role of cocaine in targeting monoamine transporters. We further show that the behavioral response to cocaine is primarily mediated by the ionotropic serotonin receptor MOD-1. Thus, cocaine modulates locomotion behavior in C. elegans primarily by impinging on its serotoninergic system.
Highlights
Cocaine is a plant alkaloid derived from coca plant leaves and represents a major drug of abuse
We find that acute cocaine treatment alters its locomotor activity
We further show that the response to cocaine in C. elegans requires the ionotropic serotonin receptor MOD-1
Summary
Cocaine is a plant alkaloid derived from coca plant leaves and represents a major drug of abuse. Cocaine elevates extracellular monoamine levels by inhibiting monoamine reuptake transporters, including DAT, SERT and NET [2,3]. By acting on their cognate receptors, monoamines elicit both short-term and long-lasting alterations in the nervous system, which lead to the development of drug dependence [4]. To better understand the mechanistic underpinnings of drug addiction, and to develop new therapeutic interventions, a greater knowledge of the genes and molecules regulating cocaine’s behavioral effects is required
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