Throughout this discussion, we will sometimes use the acronym L-HPA. The “L” in this case stands for limbic and conveys the importance of limbic system in regulation of HPA responses to psychological stressors (see review, Herman et al., 2005). Activation of the HPA axis to psychological stressors involves the amygdala and perhaps the infralimbic cortex, while inhibition of the HPA response involves the hippocampus and medial prefrontal cortex (Diorio et al., 1993; Herman et al., 2005; Sullivan and Gratton, 2002). These limbic sites have minimal direct projections to CRH-producing regions in the hypothalamus. Instead, they relay to these neurons via neurons in the bed nucleus of the stria terminalis and regions in the hypothalamus and brainstem that have access to hypothalamic CRH-producing neurons. The central nucleus of the amygdala also has projections to brainstem regions which activate sympatho-adrenal responses to stressors (Pitkanen et al., 1997). Thus, HPA and sympatho-adrenal activational pathways overlap with the threat-response system described next.
