press trust of india
WASHINGTON, 25 JUNE: Researchers have identified and deactivated a brain pathway linked to cravings for alcohol in rats, a finding that could lead to treatment for alcohol abuse disorders.
Scientists at the Ernest Gallo Clinic and Research Center at University of California, San Francisco were able to prevent the addicted animals from seeking alcohol and drinking it, the equivalent of relapse.
“One of the main causes of relapse is craving, triggered by the memory by certain cues like going into a bar, or the smell or taste of alcohol,” said lead author Segev Barak.
“We learned that when rats were exposed to the smell or taste of alcohol, there was a small window of opportunity to target the area of the brain that reconsolidates the memory of the craving for alcohol and to weaken or even erase the memory, and thus the craving,” he said.
In the first phase of the study, rats had the choice to freely drink water or alcohol over the course of seven weeks, and during this time developed a high preference for alcohol.
In the next phase, they had the opportunity to access alcohol for one hour a day, which they learned to do by pressing a lever. They were then put through a 10-day period of abstinence from alcohol. Following this period, the animals were exposed for five minutes to just the smell and taste of alcohol, which cued them to remember how much they liked drinking it.
The researchers then scanned the animals’ brains, and identified the neural mechanism responsible for the reactivation of the memory of the alcohol a molecular pathway mediated by an enzyme known as mammalian target of rapamycin complex 1 (mTORC1).
They found that just a small drop of alcohol presented to the rats turned on the mTORC1 pathway specifically in a select region of the amygdala, a structure linked to emotional reactions and withdrawal from alcohol, and cortical regions involved in memory processing.
They further showed that once mTORC1 was activated, the alcohol-memory stabilised and the rats relapsed on the following days, meaning in this case, that they started again to push the lever to dispense more alcohol.
“The smell and taste of alcohol were such strong cues that we could target the memory specifically without impacting other memories, such as a craving for sugar,” said Barak.
The researchers then set out to see if they could prevent the reconsolidation of the memory of alcohol by inhibiting mTORC1, thus preventing relapse.
When mTORC1 was inactivated using a drug called rapamycin, administered immediately after the exposure to the cue (smell, taste), there was no relapse to alcohol-seeking the next day.