About 8 million Americans suffer from nightmares and flashbacks to a traumatic event. This condition, known as post-traumatic stress disorder (PTSD), is particularly common among soldiers who have been in combat, though it can also be triggered by physical attack or natural disaster.

 The researchers found that animals who underwent chronic stress prior to atraumatic experience engaged a distinctive brain pathway that encodes traumatic memories more strongly than in unstressed animals.

The researchers focused on the amygdala, an almond-sized brain structure whose functions include encoding fearful memories. They found that in animals that developed PTSD symptoms following chronic stress and a traumatic event, serotonin promotes the process of memory consolidation. When the researchers blocked amygdala cells' interactions with serotonin after trauma, the stressed animals did not develop PTSD symptoms. Blocking serotonin in unstressed animals after trauma had no effect.

Memory consolidation is the process by which short-term memories are converted into long-term memories and stored in the brain. Some memories are consolidated more strongly than others. 

Researchers discovered that chronic stress causes cells in the amygdala to express many more 5-HT2C receptors, which bind to serotonin. Then, when a traumatic experience occurs, this heightened sensitivity to serotonin causes the memory to be encoded more strongly, which authors believe contributes to the strong flashbacks that often occur in patients with PTSD.

The Food and Drug Administration has already approved a drug called agomelatine that blocks this type of serotonin receptor and is used as an antidepressant.
 
Such a drug might also be useful to treat patients who already suffer from PTSD. These patients' traumatic memories are already consolidated, but some research has shown that when memories are recalled, there is a window of time during which they can be altered and reconsolidated. It may be possible to weaken these memories by using serotonin-blocking drugs to interfere with the reconsolidation process, says the author, who plans to begin testing that possibility in animals.
 
The findings also suggest that the antidepressant Prozac and other selective serotonin reuptake inhibitors (SSRIs), which are commonly given to PTSD patients, likely do not help and may actually worsen their symptoms. Prozac enhances the effects of serotonin by prolonging its exposure to brain cells. While this often helps those suffering from depression, "There's no biological evidence to support the use of SSRIs for PTSD," author says.

http://www.biologicalpsychiatryjournal.com/article/S0006-3223(15)00533-8/abstract