Cortisol: friend or foe in the development of PTSD-associated synaptic plasticity in the amygdala?

Post-traumatic stress disorder (PTSD) is a complex and debilitating psychiatric condition, associated with distinct
changes in a region of the brain called the amygdala. These changes are associated with the recurrent ‘flashback’
experiences caused by the formation of pathologically strong fear memories. The human stress hormone cortisol
plays a role in inducing these brain changes; however, evidence also suggests that cortisol may protect against
these changes altogether. The exact role of cortisol in mediating PTSD-associated changes in the sensing nuclei
of the amygdala is unclear, but this must be established if we hope to take advantage of this process
therapeutically. Therefore, the following article reviews the evidence for the mechanism explaining the
connection between cortisol and PTSD, drawing from relevant clinical and animal model literature.
Cortisol was found to have the potential to both exacerbate and prevent the development of PTSD behaviour and
brain changes. The mechanism by which cortisol mediates these changes upon brain cells is complex and it
involves interaction with several other chemical brain signals. Understanding this mechanism and its appropriate
timings further will aid the development of preventative therapies for PTSD, and insight into fear memory
formation as a whole.