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dc.contributor.authorKalin, N H
dc.contributor.authorShelton, S E
dc.contributor.authorEngeland, C G
dc.contributor.authorHaraldsson, H M
dc.contributor.authorMarucha, P T
dc.date.accessioned2010-09-03T13:56:28Z
dc.date.available2010-09-03T13:56:28Z
dc.date.issued2010-09-03T13:56:28Z
dc.identifier.citationBrain Behav Immun. 2006, 20(6):564-8en
dc.identifier.issn08891591
dc.identifier.doi10.1016/j.bbi.2006.01.003
dc.identifier.urihttp://hdl.handle.net/2336/110660
dc.descriptionNeðst á síðunni er hægt að nálgast greinina í heild sinni með því að smella á hlekkinn Skoða/Opna(view/open)en
dc.description.abstractStress impairs healing and in part this effect is thought to be mediated by glucocorticoids. However, the brain systems that underlie the effects of stress on healing remain to be determined. Since the central nucleus of the amygdala (CeA) plays a role in mediating an individual's behavioral and physiological reactivity to stress, we investigated, in rhesus monkeys, whether selective lesions of the CeA altered the gene expression of chemokines (IL-8 and MIP-1α) that are associated with early dermal healing. We used rhesus monkeys because they provide an excellent animal model to investigate brain mechanisms relevant to human stress, anxiety, and psychopathology. Hypothalamic-pituitary-adrenal (HPA) activity was assessed in the monkeys prior to the wound healing experiment demonstrating that the CeA lesions reduce HPA activity. In the healing experiment, stress decreased IL-8 and MIP-1α gene expression in both CeA lesioned and non-lesioned animals. Conversely, the CeA lesions increased the tissue expression of IL-8 and MIP-1α mRNA prior to and after stress exposure. These results demonstrate that in primates the CeA is a key brain region involved in the regulation of processes associated with wound healing. Because of brain and behavioral similarities between rhesus monkeys and humans, these results are particularly relevant to understanding brain mechanisms that influence healing in humans.
dc.language.isoenen
dc.publisherAcademic Pressen
dc.relation.urlhttp://dx.doi.org/10.1016/j.bbi.2006.01.003en
dc.subject.meshWound Healingen
dc.subject.meshStress, Psychologicalen
dc.subject.meshMacaca mulattaen
dc.titleStress decreases, while central nucleus amygdala lesions increase, IL-8 and MIP-1α gene expression during tissue healing in non-human primatesen
dc.typeArticleen
dc.identifier.journalBrain, Behavior, and Immunityen
html.description.abstractStress impairs healing and in part this effect is thought to be mediated by glucocorticoids. However, the brain systems that underlie the effects of stress on healing remain to be determined. Since the central nucleus of the amygdala (CeA) plays a role in mediating an individual's behavioral and physiological reactivity to stress, we investigated, in rhesus monkeys, whether selective lesions of the CeA altered the gene expression of chemokines (IL-8 and MIP-1α) that are associated with early dermal healing. We used rhesus monkeys because they provide an excellent animal model to investigate brain mechanisms relevant to human stress, anxiety, and psychopathology. Hypothalamic-pituitary-adrenal (HPA) activity was assessed in the monkeys prior to the wound healing experiment demonstrating that the CeA lesions reduce HPA activity. In the healing experiment, stress decreased IL-8 and MIP-1α gene expression in both CeA lesioned and non-lesioned animals. Conversely, the CeA lesions increased the tissue expression of IL-8 and MIP-1α mRNA prior to and after stress exposure. These results demonstrate that in primates the CeA is a key brain region involved in the regulation of processes associated with wound healing. Because of brain and behavioral similarities between rhesus monkeys and humans, these results are particularly relevant to understanding brain mechanisms that influence healing in humans.


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