Abstract
We previously showed that an acute stress-induced an early corticosterone rise in the dorsal hippocampus (dHPC) and a delayed one in the ventral hippocampus (vHPC). Congruently, we hypothesized that the dHPC may influence the time-course evolution of poststress glucocorticoid rise in the vHPC. To probe this issue, we performed ibotenic acid lesions of the dHPC and measured by microdialysis the time-course evolution of corticosterone rise in the vHPC after an acute stress delivery. In nonstress condition, we showed that the dHPC lesion induced a significant increase of corticosterone both in plasma and in the vHPC. In addition, an acute stress (electric footshocks) induced a faster and more sustained corticosterone rise in the vHPC of dHPC-lesioned animals, as compared to sham-operated ones. This study provides new found evidence to the effect that the dHPC lesion alters the time-course evolution of corticosterone rise within the vHPC after stress.
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