The central administration of corticotropin-releasing hormone (CRH) to experimental
animals sets into motion a coordinated series of physiological and behavioral events
that promote survival during threatening situation. A large body of evidence suggest
that CRH in the central nucleus of the amygdala (CEA) induces fear-related behaviors
and is essential to fear conditioning; however, evidence of CRH-mediated activation
of the amygdala under physiological situation is still limited. We report here a study
of the impact of a psychological stressor on hypothalamic and amygdala CRH systems
in the rat. Non-footshocked rats placed in a floored compartment surrounded by footshocked
rats were defined as the psychological stress group. Rats were exposed to psychological
stress for 15 min, and then sacrificed 1.5 and 3 h after cessation of stress. We found
that our psychological stressor induced an increase in both CRH mRNA levels, as assessed
by in situ hybridization histochemistry, and CRH content, as assessed by micropunch
RIA, in the CEA. Exposure to the psychological stressor also caused a significant
increase in CRH mRNA levels with a trend for an increase in CRH content in the dorsolateral
subdivision of the bed nucleus of the stria terminalis (BNST) which is anatomically
associated with the CEA. In contrast, psychological stress induced a small, but significant
increase in type-1 CRH receptor (CRHR-1) mRNA in the hypothalamic paraventricular
nucleus (PVN), while it failed to elevate either PVN CRH mRNA levels or content, CRH
content in the median eminence (ME), or levels of plasma ACTH or corticosterone (CORT).
Thus, in the context of a psychological stressor, the activation of the amygdala CRH
system can occur without robust activation of the hypothalamic CRH system. In the
light of previous data that the psychological stress-induced loss of sleep was reversed
by the central administration of a CRH antagonist, these data suggest that CRH in
the CEA may contribute to the psychological stress-evoked fear-related behavior such
as hyperarousal. These data also indicate that in response to a psychological stressor,
the amygdala CRH system is much more sensitive than is the CRH system emanating from
the PVN.