How Brains Remember Pleasure: Drug Addiction Different from Reward Memories

When the brain remembers pleasure, it sparks nerve cells that are different from the ones associated with drug addiction. Now, scientists have taken a closer look at the molecular events that form such "reward memories," which could allow them to better understand addiction.

Brain circuits evolved to encourage behaviors proven to help our species survive by attaching pleasure to them. For example, eating rich food tastes good since it delivers energy. The same systems also connect in our mind's environmental cues with actual pleasures to form reward memories. In order to learn a little bit more about these systems, the scientists took a look at rats.

The brain's pleasure center is known to proceed through nerve cells that signal using the neurochemical dopamine and generally is located in the ventral tegmental area (VTA), which is a region of the brain. Dopaminergic neurons exhibit a remarkable capacity to pass along pleasure signals. Unfortunately, the evolutionary processes that attached pleasure to advantageous behaviors also reinforced bad ones--like addiction to major classes of abused drugs. In fact, addiction to all four major classes of these drugs has been linked to increased dopamine transmission in the same parts of the brain associated with normal reward processing.

In this study, the scientists trained rats to associate a sound tone with the availability of sugar pellets in their feed ports. In order to separate the effects of memory-related brain changes from those arising from the pleasure of eating itself, the rats were then separated into three groups. One group got sugar pellets each time they heard a sound cue, the second group heard the sound the same number of times and received as many sugar pellets--but never together and a third tone-only group heard the sounds but never received rewards.

So what did they find? It turns out that the rats that always received sugar poked their feed ports with their noses at least twice as often during this cue as control rats. In addition, the rats in this group that were better at forming reward memories had significantly higher expression of the genes Egr1 and Fos than control rats. These genes are known to regulate memory in other brain regions by fine-tuning the signaling capacity of the connections between nerve cells. In the end, the researchers found that reward-related experiences caused both types of DNA methylation known to regulate gene expression.

"We observed an important distinction, no in circuitry, but instead in the epigenetic regulation of that circuitry between natural reward responses and those that occur downstream with drugs of abuse or psychiatric illness," said Jeremy Day, one of the researchers, in a news release. "Although drug experiences may co-opt normal reward mechanisms to some extent, our results suggest they also may engage entirely separate epigenetic mechanisms that contribute only to addiction and that may explain its strength."

The findings could allow researchers to develop better therapeutic treatments for those with addictions. More specifically, the study reveals that future treatments could dial down addiction or mental illness without affecting normal rewards. This could greatly benefit patients.

The findings are published in the journal Nature Neuroscience.