Understanding the Brain’s Functions in Addiction

Previous research has shown that many of the same brain functions activated in those with drug addictions are similar to those who struggle with disordered eating behaviors. Reward receptors seem to be malfunctioning when people are addicted to substances that are associated with the release of dopamine in the brain.

While the general perception may be that those with binge eating disorder, bulimia or a problem with obesity love to eat, the reverse may be true. Those with eating disorders may in fact be enjoying their food less than healthy individuals because their reward receptors do not function properly.

A recent study conducted at Uppsala University examined the brain’s response to rewards in relation to the co-signaling of glutamate and dopamine. Led by Associate Professor of Neuroscience Asa Mackenzie, the study sought to investigate how the brain’s normal reward response can be “kidnapped” by certain substances like alcohol and cocaine.

The brain’s reward system is activated when we have eaten something we enjoy or had sex, for instance, and the pleasure is experienced because certain substances in the brain like dopamine are released. However, this system can be thrown off track by other rewarding substances, like alcohol or drugs. While these substances create an initial reward response, the reactions are so strong that nerve cells become rewired and addiction begins. Foods high in sugar can also produce the same result.

The Uppsala study provided evidence that dopamine cells in the brain can send signals in cooperation with glutamate, a process called co-signaling.

Studies of mice with glutamate transporters unable to perform co-signaling functions gave researchers an opportunity to examine how the mice reacted to opportunities to ingest reward substances, such as sugar or cocaine. The results of the analysis showed that the mice ingested more and responded to lower dosages when compared with control mice.

The researchers also investigated the connection between memory and consumption of substances. Mice that lack the ability to co-signal developed significant improvement in the memory of environments associated with the opportunity to obtain drugs. There were also observations made that changes in genetic expressions in the reward system indicate that the brain has become hypersensitive and that dopamine levels had decreased.

The information gained by the study may be helpful in the development of medications that address the challenges of both drug addiction and eating disorders. However, Mackenzie cautions that while the results are intriguing, further research is necessary to understand how drug development may be impacted by the knowledge of co-signaling.