Early-life stress produces a cascade of neurobiological events that cause enduring changes in neural plasticity and synaptic efficacy that appear to play pivotal roles in the pathophysiology of
post-traumatic stress disorder (
PTSD).
Brain-derived neurotrophic factor (
BDNF) has been implicated in the neurobiological mechanisms of these changes, in interaction with components of the stress response, such as
corticosterone. This study examined the consequences of juvenile stress for behavior during adulthood in association with circulating
corticosterone levels and
BDNF expression. The experiments examined single exposure to predator scent stress (soiled cat litter for 10 min) as compared to repeated exposure, early in life and later on. Behavioral responses were assessed in the elevated plus maze and the acoustic startle response paradigms at 28, 60 and 90 days of age. Plasma
corticosterone was measured and brain areas analyzed for
BDNF levels. The results show that juvenile stress exposure increased anxiety-like behavior and startle amplitude and decreased plasma
corticosterone. This response was seen immediately after exposure and also long term. Adult stress exposure increased anxiety-like behavior, startle amplitude and plasma
corticosterone. Exposure to both early and later life
trauma elicited reduced levels of
corticosterone following the initial exposure, which were not raised by re-exposure, and elicited significant downregulation of
BDNF mRNA and
protein levels in the hippocampus CA1 subregion. The consequences of adult stress exposure were more severe in rats were exposed to the same stressor as juveniles, indicated increased vulnerability. The results suggest that juvenile stress has resounding effects in adulthood reflected in behavioral responses. The concomitant changes in
BDNF and
corticosterone levels may mediate the changes in neural plasticity and synaptic functioning underlying clinical manifestations of
PTSD.