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Evidence that the bed nucleus of the stria terminalis contributes to the modulation of hypophysiotropic corticotropin-releasing factor cell responses to systemic interleukin-1β

Crane, James W., Buller, Kathryn M. and Day, Trevor A. 2003, Evidence that the bed nucleus of the stria terminalis contributes to the modulation of hypophysiotropic corticotropin-releasing factor cell responses to systemic interleukin-1β, Journal of comparative neurology, vol. 467, no. 2, pp. 232-242, doi: 10.1002/cne.10918.

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Title Evidence that the bed nucleus of the stria terminalis contributes to the modulation of hypophysiotropic corticotropin-releasing factor cell responses to systemic interleukin-1β
Author(s) Crane, James W.
Buller, Kathryn M.
Day, Trevor A.
Journal name Journal of comparative neurology
Volume number 467
Issue number 2
Start page 232
End page 242
Total pages 11
Publisher Wiley
Place of publication London, England
Publication date 2003-12-08
ISSN 0021-9967
1096-9861
Keyword(s) BNST
central amygdala
ACTH
Fos
Summary Systemic infection activates the hypothalamic-pituitary-adrenal (HPA) axis, and brainstem catecholamine cells have been shown to contribute to this response. However, recent work also suggests an important role for the central amygdala (CeA). Because direct connections between the CeA and the hypothalamic apex of the HPA axis are minimal, the present study investigated whether the bed nucleus of the stria terminalis (BNST) might act as a relay between them. This was done by using an animal model of acute systemic infection involving intravascular delivery of the proinflammatory cytokine interleukin-1β (IL-1β, 1 μg/kg). Unilateral ibotenic acid lesions encompassing the ventral BNST significantly reduced both IL-1β-induced increases in Fos immunoreactivity in corticotropin-releasing factor (CRF) cells of the hypothalamic paraventricular nucleus (PVN) and corresponding increases in adrenocorticotropic hormone (ACTH) secretion. Similar lesions had no effect on CRF cell responses to physical restraint, suggesting that the effects of BNST lesions were not due to a nonspecific effect on stress responses. In further studies, we examined the functional connections between PVN, BNST, and CeA by combining retrograde tracing with mapping of IL-1β-induced increases in Fos in BNST and CeA cells. In the case of the BNST, these studies showed that systemic IL-1β administration recruits ventral BNST cells that project directly to the PVN. In the case of the CeA, the results obtained were consistent with an arrangement whereby lateral CeA cells recruited by systemic IL-1β could regulate the activity of medial CeA cells projecting directly to the BNST. In conclusion, the present findings are consistent with the hypothesis that the BNST acts as a relay between the CeA and PVN, thereby contributing to CeA modulation of hypophysiotropic CRF cell responses to systemic administration of IL-1β.
Language eng
DOI 10.1002/cne.10918
Field of Research 060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970106 Expanding Knowledge in the Biological Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2003, Wiley-Liss
Persistent URL http://hdl.handle.net/10536/DRO/DU:30044494

Document type: Journal Article
Collection: Faculty of Science, Engineering and Built Environment
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