Prl Cortex: A Case Study

a) Medial prefrontal cortex: the mPFC is divided into three subregions, which have differential control over HPA axis. The prelimbic (PrL) and anterior cingulate cortex (ACC) provides negative feedback to HPA axis and thereby reduces the stress-induced activation of HPA axis. The PrL and ACC reduces the duration of secretion without altering the peak of secretions and thus help in response termination. The lesion of mPFC consisting prelimbic cortex have known to produced enhanced cfos expression in paraventricular nucleus of stressed animals as compared to control, which also parallels with higher circulating ACTH levels in lesioned animals (Helmer F. Figueiredo et al., 2003, Radley et al., 2006). Another study by Diorio et al. 1993 shows the …show more content…
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