Abstract
Stress can lead to a wide variety of psychiatric illnesses such as major depressive disorder (MDD) and post-traumatic stress disorder (PTSD). However, some individuals are more susceptible to developing psychopathology in response to stress, while others exhibit stress resilience; yet, the research into the underlying neurobiology of this phenomenon is still in its infancy. We have previously shown that (R,S)-ketamine can buffer fear expression and that this effect is partially mediated by activity in the ventral CA3 (vCA3) subregion of the hippocampus. However, it is unknown how exactly activity is changed, particularly in vCA3, during prophylactic ketamine treatment, stress, or expression of depressive-like or fear behaviors.
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