Repeated stress induces
corticosterone release. However, it is not clear that stress results in further elevation of
corticosterone levels, and the roles of released
corticosterone to aggravate stress-related symptoms are also not clear. This study investigated whether neuronal modulation was induced in the amygdala after two kinds of stress, that is, such as electric
shock and
corticosterone injection. It was found that stress by electric
shock decreased the expression of
tyrosine hydoroxylase (TH) in the amygdala while the expression of pERK was increased. However, there is no difference in the expressions of TH and pERK in the frontal cortex compared with those of the control group. The level of
corticosterone was significantly increased in the serum after stress. To determine the effect of
corticosterone on the induction of anxiety and the expression of TH, the rats received
corticosterone (20 mg or 40 mg/kg i.p.) for 1 day, 1 week, 2 weeks and 3 weeks, respectively. The spent time in open arms of the EPM (elevated plus maze) test was significantly decreased after 1 week, 2 weeks and 3 weeks. The time spent in open arms of the EPM test after repeated
injections of
corticosterone was significantly decreased in a dose-dependent manner. The expression of TH in the amygdala was reduced after following repeated
corticosterone treatment for 2 weeks and 3 weeks. Collectively, this study suggests that
corticosterone has a major role in the induction of anxiety and the modulation of TH expression, at least, in the amygdala.