Hippocampal lesion augments the stress-induced enhanced secretion of plasma corticosterone (Sapolsky RM, Krey LC, McEwen BS 1984). The hippocampus also regulates the ACTH secretion during stress and non-stressed conditions (Knigge KM, Hays M 1963). Similarly, the stimulation of hippocampus causes decline in stress-induced release of ACTH and glucocorticoids in both rodents (Dupont A, Bastarache E, Endroczi E, Fortier C 1972; Kawakami M, Seto K, Terasawa E, Yoshida K, Miyamoto T, Sekiguchi M, Hattori Y 1968) and humans (Rubin, R. T., Mandell, A. J. & Crandall, P. H.1966). Additionally, rats with ablated hippocampi also show an enhanced activation of HPA axis following stress (Sapolsky RM, Krey LC, McEwen BS 1984; Kant GJ, Meyerhoff JL, Jarrard LE 1984). Therefore, it can be concluded the hippocampus regulates both peak as well as response termination during stressful …show more content…
Amygdala mainly consist of central nucleus (CeA), basolateral (BLA) and medial (MeA) nucleus which regulate HPA axis differentially. The CeA following stress gets activated and thus regulate the autonomic and emotional component of systemic stressors but not psychogenic stressor. However, CeA lesion impairs the bradycardic response to psychogenic stressors. The MeA and BLA gets activated following psychological stress and enhance the activity of HPA axis. Both MeA and BLA lesion decreases the stress-induced alterations in physiological and psychological functioning. The BLA lesion as well as inactivation prevents the stress induced gastric ulceration (), cognitive deficits (), hippocampal LTP ( ), dendritic retraction in CA3 fields (), neurochemical alteration ( ), GR expression in hippocampal CA1 field () and synaptophysin expression (). The effect of BLA on HPA axis is mediated by direct projections from BLA to PVN. However, some of the beneficial effect of BLA during stress are also mediated via its own afferent to dorsal CA1 region of hippocampus. Additionally, a recent study by Rei et al. demonstrated that chronic photostimulation of BLA causes stress-like behavioural and molecular changes. Therefore, BLA is a crucial target for reversal of stress-induced behavioural, molecular and morphological