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Abstract
Post-traumatic stress disorder (PTSD) is a chronic and disabling condition arising
after exposure to a severe traumatic event, which affects approximately eight percent
of the population. The underlying neurobiology of PTSD, however, has only been partially
understood. The exploration of fear memory and its extinction has been the subject
to increase our understanding of PTSD. Our previous studies have already found that
adolescent mice exhibited impaired fear memory extinction with accompanied depressive-like
behaviors. Considering the relationship between ketamine and its rapid antidepressant
function, we hypothesis that ketamine can facilitate the fear memory extinction so
as to exhibit an antidepressant effects. In this study, to evaluate our hypothesis,
we intraperitoneal (i.p.) injection of ketamine in adolescent mice and found that
ketamine exhibited a rapid antidepressant effect and facilitated the fear memory extinction.
Moreover, ketamine can also reverse the accompanied depressive-like behaviors and
restore long-term potentiation (LTP) induction in extinction process, which involved
the presynaptic mechanism. Our results suggest that ketamine exhibited an antidepressant
effect in FST and facilitated the fear memory extinction via presynaptic-mediated
synaptic plasticity, which may provide new strategy for treatment of PTSD.