A new study from Ruhr-University Bochum finds that mice without a certain serotonin receptor unlearn fear faster than those with it. These findings may be helpful in understanding the mechanisms of current drugs to treat post-traumatic stress disorder (PTSD) as well as help researchers improve those drugs. The research was published in Translational Psychiatry in November.
PTSD can become very difficult—in some cases impossible—to treat with therapies because the neurological connection between an environmental stimulus and the learned, exaggerated fear response runs so deep. Previous literature has established that the serotonin transmitter plays a role in fear response regulation. Knowing this, study authors Katharina Spoida and Sandra Süß dug into the underlying neurochemical mechanisms behind that regulation. They found that mice genetically modified to have no 5-HT2C serotonin receptor “unlearned” fear responses much faster than mice who were not genetically modified.
To instill fear in the mice, they played a specific sound while giving the mice light electric shocks. The next day, both the engineered mice and the wild mice would freeze every time the tone played even without an electric shock. However, the engineered learned to dissociate the past electric shocks from the tone much faster than the wild mice. “Consequently,” said Spoida, “it looks like the absence of the serotonin receptor provides an advantage for extinction learning.”
The researchers then found that the engineered mice had changes in neuronal activity in two different brain regions. One region was the main production center for serotonin. The other was in the extended amygdala, which also plays a role in extinction learning, which is the gradual lessening in response to a stimulus presented without reinforcement.
These findings may illuminate how current drugs used to treat PTSD affect those two regions of the brain and, ideally, can be used in developing new, more targeted treatment plans for PTSD patients.