Activation of the central amygdala (CeA) by
corticosterone (CORT) induces somatic and colonic
hypersensitivity through
corticotrophin-releasing factor (CRF)-dependent mechanisms. However, the importance of the bed nucleus of the stria terminalis (BNST), part of the extended amygdala, on nociception remains unexplored. In the present study, we test the hypothesis that stimulation of the CeA by CORT induces somatic and colonic
hypersensitivity through activation of the anteriolateral BNST (BNST(AL)). Animals were implanted with micropellets of CORT or
cholesterol (CHOL) onto the CeA or the BNST(AL). Mechanical sensitivity was quantified using electronic von Frey filaments, and colonic nociception was measured by quantifying a visceromotor response to graded colorectal distension. In situ hybridization was used to determine
mRNA levels for CRF, CRF(1), and CRF(2) receptors in the BNST(AL). In a second group, animals were implanted bilaterally with 1) CORT or CHOL micropellets onto the CeA; and 2) cannulas localized to the BNST(AL) to administer a CRF(1) receptor antagonist (
CP376395). Animals implanted with CORT onto the CeA, but not the BNST(AL), exhibited increased expression of CRF
mRNA and increased CRF(1)-to-CRF(2) receptor ratio in the BNST, as well as somatic and colonic
hypersensitivity compared with CHOL controls. Infusion of
CP376395 into the BNST(AL) inhibited somatic and colonic
hypersensitivity in response to elevated amygdala CORT. Somatic and colonic
hypersensitivity induced by elevated amygdala CORT is mediated via a CRF(1) receptor-dependent mechanism in the BNST(AL). The CeA through a descending pathway involving the BNST(AL) plays a pivotal role in somatic and colonic nociception.