For decades, neuroscientists have studied how cocaine affects the brain in hopes of developing medications to prevent cocaine addiction. To date, however, none have been approved by the US Food and Drug Administration.

Cocaine is generally thought to produce its rewarding effects by increasing levels of the chemical messengers dopamine and serotonin within the brain. Medications that block these chemical messengers, however, have demonstrated limited efficacy in clinical trials, suggesting that cocaine may affect other chemical messengers as well. 

Recently, I and my fellow researchers at Davidson College published study results which suggest that cocaine may target an additional chemical messenger called acetylcholine. In the study, we administered cocaine to small nematode worms often used to study human biology called Caenorhabditis elegans. We observed that cocaine caused the worms to lay eggs. Next, we tested which chemical messengers had to be present in the brain circuit that controls worm egg laying, to make the link between cocaine and egg laying behavior. We found that acetylcholine is necessary for cocaine to cause worm egg laying, suggesting that cocaine might increase acetylcholine signaling.

Additional research in other animals such as rats and mice, and eventually humans, is necessary to find out if cocaine can increase acetylcholine signaling in the brain to cause addiction. If this is the case, however, then neuroscientists may be able to design medications that block acetylcholine to prevent cocaine addiction.