A new study from the Ruhr-University Bochum finds that mice without a certain serotonin receptor unlearn fear faster than those with it. These findings may be useful in understanding the mechanisms of current medications to treat post-traumatic stress disorder (PTSD), as well as in helping researchers improve those medications. 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 regulating the fear response. Knowing this, study authors Katharina Spoida and Sandra Süß investigated the underlying neurochemical mechanisms behind that regulation. They found that mice genetically modified to lack a serotonin 5-HT2C receptor responded to “unlearned” fear much faster than mice that were not genetically modified.
To instill fear in the mice, they played a specific sound while giving them light electric shocks. The next day, both modified and wild-type mice froze whenever the tone sounded, even without an electric shock. However, the engineer learned to dissociate past electrical discharges from tone much faster than wild mice. “Due,” Spoida said“It appears that the absence of the serotonin receptor provides an advantage for extinction learning.”
The researchers then found that the modified mice had changes in neural activity in two different brain regions. One region was the main center of serotonin production. The other was in the extended tonsil, which also plays a role in extinction learningwhich is the gradual decrease in response to a stimulus presented without reinforcement.
These findings may shed light on how current medications used to treat PTSD affect these two brain regions, and ideally can be used to develop new, more targeted treatment plans for PTSD patients.
